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Nutrients, Volume 9, Issue 4 (April 2017) – 107 articles

Cover Story (view full-size image): Orally administered sea buckthorn pulp oil (not seed oil) restored aqueous tear secretion to its normal value under a dry eye condition. Palmitoleate (C16:1), a fatty acid present in sea buckthorn pulp oil, preserved tear secretion and suppressed inflammatory cytokines in the lacrimal gland to the same extent as that by pulp oil. These results suggest that an oral intake of sea buckthorn pulp oil has a potency to preserve tear secretion capacity in the dry eye state and palmitoleate, its main constituent fatty acid, is an active component of the oil. This effect may enable a potent diet-based treatment for the prevention of dry eye. View the paper
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0 pages, 150 KiB  
Retraction
RETRACTED: Yu et al. Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats. Nutrients 2016, 8, 456
by Nutrients Editorial Office
Nutrients 2017, 9(4), 422; https://doi.org/10.3390/nu9040422 - 25 Apr 2017
Viewed by 4290
Abstract
The Nutrients Editorial Office has recently been made aware that the figures in the title paper [1] are taken from the same micrographs as those of other papers by the same authors [...] Full article
1829 KiB  
Article
Supplementation with a Polyphenol-Rich Extract, PerfLoad®, Improves Physical Performance during High-Intensity Exercise: A Randomized, Double Blind, Crossover Trial
by Julien Cases, Cindy Romain, Cristian Marín-Pagán, Linda H. Chung, José Miguel Rubio-Pérez, Caroline Laurent, Sylvie Gaillet, Emmanuelle Prost-Camus, Michel Prost and Pedro E. Alcaraz
Nutrients 2017, 9(4), 421; https://doi.org/10.3390/nu9040421 - 24 Apr 2017
Cited by 28 | Viewed by 13238
Abstract
Workout capacity is energy-production driven. To produce peak metabolic power outputs, the organism predominantly relies more on anaerobic metabolism, but this undoubtedly has a negative and limiting impact on muscle function and performance. The aim of the study was to evaluate if an [...] Read more.
Workout capacity is energy-production driven. To produce peak metabolic power outputs, the organism predominantly relies more on anaerobic metabolism, but this undoubtedly has a negative and limiting impact on muscle function and performance. The aim of the study was to evaluate if an innovative polyphenol-based food supplement, PerfLoad®, was able to improve metabolic homeostasis and physical performance during high-intensity exercises under anaerobic conditions. The effect of a supplementation has been investigated on fifteen recreationally-active male athletes during a randomized, double-blind and crossover clinical investigation. The Wingate test, an inducer of an unbalanced metabolism associated to oxidative stress, was used to assess maximum anaerobic power during a high-intensity exercise on a cycle ergometer. Supplementation with PerfLoad® correlated with a significant increase in total power output (5%), maximal peak power output (3.7%), and average power developed (5%), without inducing more fatigue or greater heart rate. Instead, oxidative homeostasis was stabilized in supplemented subjects. Such results demonstrated that PerfLoad® is a natural and efficient solution capable of, similarly to training benefits, helping athletes to improve their physical performance, while balancing their metabolism and reducing exercise-induced oxidative stress. Full article
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<p>HPLC polyphenolic profile of the supplement at 260, 280, and 310 nm (A = bioflavonoids; B = punicalagins; C = gallic acid; D = trans-resveratrol; E = caffeine).</p>
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<p>CONSORT (Consolidated Standards of Reporting Trials) flowchart of participants during the study intervention.</p>
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<p>Anaerobic mechanical power (W) developed during a 30-s Wingate bout and representing the total anaerobic work capacity (J/30 s). Values are means ± SD, <span class="html-italic">n</span> = 15 (placebo) or <span class="html-italic">n</span> = 15 (PerfLoad<sup>®</sup>). * Superscript indicates an intergroup difference between PerfLoad<sup>®</sup> and placebo, <span class="html-italic">p</span> &lt; 0.05.</p>
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<p>Blood pulse pressure (mmHg) measured 60 min before and just before (Pre-exercise), just before and just after (Exercise), just after and 60 min after (Post-exercise) a 30-s Wingate bout. Values are means ± SD, <span class="html-italic">n</span> = 15 (placebo) or <span class="html-italic">n</span> = 15 (PerfLoad<sup>®</sup>). * Superscript indicates an intergroup difference between PerfLoad<sup>®</sup> and placebo, <span class="html-italic">p</span> &lt; 0.05.</p>
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<p>KRL and RESEDA global antioxidant protection of red blood cells (RBCs) (arbitrary units) measured 60 min before and just before (Pre-exercise), just before and just after (Exercise), and just after and 60 min after (Post-exercise) a 30-s Wingate bout. Values are means ± SD, <span class="html-italic">n</span> = 15 (placebo) or <span class="html-italic">n</span> = 15 (PerfLoad<sup>®</sup>). * Superscript indicates an intergroup difference between PerfLoad<sup>®</sup> and placebo, <span class="html-italic">p</span> &lt; 0.05.</p>
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<p>SOD (<b>A</b>), GSH-PX (<b>B</b>), Cat (<b>C</b>), and LDH (<b>D</b>) activities measured just before (Pre-exercise), just after (Exercise), and 60 min after (Post-exercise) a 30-s Wingate bout. Values are means ± SD, <span class="html-italic">n</span> = 15 (placebo) or <span class="html-italic">n</span> = 15 (PerfLoad<sup>®</sup>). * Superscript indicates an intergroup difference between PerfLoad<sup>®</sup> and placebo, <span class="html-italic">p</span> &lt; 0.05.</p>
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1248 KiB  
Article
Associations between Diet and Toenail Arsenic Concentration among Pregnant Women in Bangladesh: A Prospective Study
by Pi-I. D. Lin, Sabri Bromage, Md. Golam Mostofa, Joseph Allen, Emily Oken, Molly L. Kile and David C. Christiani
Nutrients 2017, 9(4), 420; https://doi.org/10.3390/nu9040420 - 23 Apr 2017
Cited by 12 | Viewed by 7007
Abstract
This prospective study evaluated the relationship between long-term dietary habits and total arsenic (As) concentration in toenail clippings in a cohort of 1616 pregnant women in the Bangladeshi administrative regions of Sirajdikhan and Pabna Sadar. Diet was assessed at Gestation Week 28 and [...] Read more.
This prospective study evaluated the relationship between long-term dietary habits and total arsenic (As) concentration in toenail clippings in a cohort of 1616 pregnant women in the Bangladeshi administrative regions of Sirajdikhan and Pabna Sadar. Diet was assessed at Gestation Week 28 and at Postpartum Month 1, using a locally-validated dish-based semi-quantitative food-frequency questionnaire. Toenail As concentration was analyzed by microwave-assisted acid digestion and inductively coupled plasma mass spectrometry. Associations between natural log-transformed consumption of individual food items and temporally matched natural log-transformed toenail As concentration were quantified using general linear models that accounted for As concentration in the primary drinking water source and other potential confounders. The analysis was stratified by As in drinking water (≤50 μg/L versus >50 μg/L) and the time of dietary assessment (Gestation Week 28 versus Postpartum Week 1). Interestingly, toenail As was not significantly associated with consumption of plain rice as hypothesized. However, toenail As was positively associated with consumption of several vegetable, fish and meat items and was negatively associated with consumption of rice, cereal, fruits, and milk based food items. Further studies in pregnant women are needed to compare As metabolism at different levels of As exposure and the interaction between dietary composition and As absorption. Full article
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<p>Study flow chart.</p>
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<p>Associations between natural log-transformed food intake (g/day) and natural log-transformed toenail As concentration (μg/g) measured by the first and the second dietary assessment (FFQ1 and FFQ2, respectively) among women exposing to drinking water As concentration of &gt;50 μg/L and ≤50 μg/L in Bangladesh. Effect size is the slope coefficients (<math display="inline"> <semantics> <mover accent="true"> <mi mathvariant="sans-serif">β</mi> <mo>^</mo> </mover> </semantics> </math>) for each dietary item and has the unit of ln((toenail As concentrations, μg/g)·(g/day)<sup>−1</sup>). “C” stands for crude model adjusted for water As concentration only; “A” stands for adjusted model adjusted for water As level, sex, smoking in the living environment, chewing betel nut, BMI, daily water intake, daily energy intake, and education level. <span class="html-italic">Q</span>-value accounting for multiple comparisons using the false discovery rate (FDR = 0.05) method. (Quantitative values presented in the <a href="#app1-nutrients-09-00420" class="html-app">Supplementary Materials, Tables S1 and S2</a>).</p>
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Article
The Reliability of the Mediterranean Diet Quality Index (KIDMED) Questionnaire
by Lovro Štefan, Rebeka Prosoli, Dora Juranko, Marko Čule, Ivan Milinović, Dario Novak and Goran Sporiš
Nutrients 2017, 9(4), 419; https://doi.org/10.3390/nu9040419 - 23 Apr 2017
Cited by 77 | Viewed by 8957
Abstract
The purpose of the present study was to determine the test–retest reliability of the Mediterranean Diet Quality Index (KIDMED) questionnaire in college students. Two hundred and seventy-six college students (127 men, 46%; 149 women, 54%; mean age 19.70 ± 1.32 years; mean height [...] Read more.
The purpose of the present study was to determine the test–retest reliability of the Mediterranean Diet Quality Index (KIDMED) questionnaire in college students. Two hundred and seventy-six college students (127 men, 46%; 149 women, 54%; mean age 19.70 ± 1.32 years; mean height 1.75 ± 0.09 m; mean weight 69.28 ± 13.84 kg; mean body-mas index 22.41 ± 3.19 kg/m2) participated in the study. To investigate the reliability of the KIDMED questionnaire, the participants were asked to complete the questionnaire on two occasions two weeks apart, stratified by gender. Kappa statistics showed moderate to excellent agreement (ranging from 0.504 to 0.849) in the total sample and moderate to excellent agreement in both men (ranging from 0.467 to 0.803) and women (ranging from 0.435 to 0.927). Results in the total KIDMED score showed a moderate correlation between two occasions inthe total sample (κ = 0.597, p < 0.001) and in women (κ = 0.586, p < 0.001) and a good correlation in men (κ = 0.611, p < 0.001). Our study shows that the KIDMED questionnaire is a reliable instrument for assessing adherence to the Mediterranean diet in college students. Future studies should focus on investigating the reliability of the questionnaire in other countries and in different age groups for generating comparable data. Full article
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Article
Sweet Taste Receptor Activation in the Gut Is of Limited Importance for Glucose-Stimulated GLP-1 and GIP Secretion
by Monika Y. Saltiel, Rune E. Kuhre, Charlotte B. Christiansen, Rasmus Eliasen, Kilian W. Conde-Frieboes, Mette M. Rosenkilde and Jens J. Holst
Nutrients 2017, 9(4), 418; https://doi.org/10.3390/nu9040418 - 22 Apr 2017
Cited by 28 | Viewed by 7990
Abstract
Glucose stimulates the secretion of the incretin hormones: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). It is debated whether the sweet taste receptor (STR) triggers this secretion. We investigated the role of STR activation for glucose-stimulated incretin secretion from an isolated perfused [...] Read more.
Glucose stimulates the secretion of the incretin hormones: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). It is debated whether the sweet taste receptor (STR) triggers this secretion. We investigated the role of STR activation for glucose-stimulated incretin secretion from an isolated perfused rat small intestine and whether selective STR activation by artificial sweeteners stimulates secretion. Intra-luminal administration of the STR agonists, acesulfame K (3.85% w/v), but not sucralose (1.25% w/v) and stevioside (2.5% w/v), stimulated GLP-1 secretion (acesulfame K: 31 ± 3 pmol/L vs. 21 ± 2 pmol/L, p < 0.05, n = 6). In contrast, intra-arterial administration of sucralose (10 mM) and stevioside (10 mM), but not acesulfame K, stimulated GLP-1 secretion (sucralose: 51 ± 6 pmol/L vs. 34 ± 4 pmol/L, p < 0.05; stevioside: 54 ± 6 pmol/L vs. 32 ± 2 pmol/L, p < 0.05, n = 6), while 0.1 mM and 1 mM sucralose did not affect the secretion. Luminal glucose (20% w/v) doubled GLP-1 and GIP secretion, but basolateral STR inhibition by gurmarin (2.5 µg/mL) or the inhibition of the transient receptor potential cation channel 5 (TRPM5) by triphenylphosphine oxide (TPPO) (100 µM) did not attenuate the responses. In conclusion, STR activation does not drive GIP/GLP-1 secretion itself, nor does it have a role for glucose-stimulated GLP-1 or GIP secretion. Full article
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<p>Glucose is a potent GLP-1 and GIP secretagogue and it is rapidly absorbed in the upper small intestine. Data is shown as averaged mean values ± SEM. (<b>a</b>) Glucose output in venous effluents in response to administration of luminal glucose. (<b>b</b>) Comparison between the venous glucose output upon glucose (stimulation) or saline (baseline). (<b>c</b>) GLP-1 (red line) and GIP (green line) secretion in response to luminal glucose. (<b>d</b>,<b>e</b>) Comparison between total GLP-1 or GIP output caused by glucose or saline. (<b>f</b>) GLP-1 (red line) and GIP (green line) secretion by luminal glucose administration and inhibition of the sweet taste receptor. (<b>g</b>,<b>h</b>) Comparison between the mean values of GLP-1 or GIP output upon glucose infusion ± gurmarin and saline. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001. BBS bombesin; GLP-1 glucagon-like peptide 1; GIP glucose-dependent insulinotropic peptide.</p>
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<p>Effects of artificial sweeteners on incretin secretion. Data is shown as averaged mean values ± SEM (<b>a</b>) GLP-1 (red line) and GIP (green line) secretion in response to luminal sucralose and acesulfame K (<b>b</b>,<b>c</b>) Comparison between total GLP-1 or GIP output caused by luminal artificial sweeteners (stimulation) and saline (baseline) (<b>d</b>) GLP-1 secretion in response to vascular sucralose and acesulfame K (<b>e</b>) Comparison between the mean values of total GLP-1 secretion caused by vascular artificial sweeteners and saline (<b>f</b>) GLP-1 output in response to luminal and vascular stevioside administration (<b>g</b>) Comparison between the mean values of GLP-1 secretion upon liminal and vascular stevioside and saline * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001. BBS bombesin; GLP-1 glucagon-like peptide 1; GIP glucose-dependent insulinotropic peptide.</p>
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<p>Effects of sucralose on the secretion of GLP-1 and GIP. Data is shown as averaged mean values ± SEM (<b>a</b>) GLP-1 secretion in response to vascular sucralose at 0.1 mM, 1 mM, and 10 mM concentrations (<b>b</b>) Comparison between the mean values of total GLP-1 output caused by vascular sucralose in increasing concentration (stimulation) and saline (baseline) (<b>c</b>) GLP-1 (red line) and GIP (green line) secretion in response to vascular administration of sucralose (<b>d</b>,<b>e</b>) Comparison between the mean values of total GLP-1 or GIP output caused by vascular sucralose and saline (<b>e</b>) GLP-1 secretion in response to vascular administration of sucralose ± gurmarin (<b>f,g</b>) Comparison between the mean values of GLP-1 output upon sucralose ± gurmarin * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001. BBS bombesin; GLP-1 glucagon-like peptide 1; GIP glucose-dependent insulinotropic peptide.</p>
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<p>TRPM5 channel is not involved in glucose- and sucralose-stimulated GLP-1 secretion. Data is shown as averaged mean values values ± SEM (<b>a</b>) GLP-1 secretion in response to luminal glucose alone or in the presence of TPPO (<b>b</b>) Comparison between the mean values of total GLP-1 output caused by luminal glucose ± TPPO (stimulation) and saline (baseline) (<b>c</b>) GLP-1 secretion in response to vascular administration of sucralose alone or in presence of TPPO (<b>d</b>) Comparison between the mean values of total GLP-1 output caused by vascular sucralose ± TPPO and saline * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001. BBS bombesin; GLP-1 glucagon-like peptide 1; GIP glucose-dependent insulinotropic peptide.</p>
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Article
Sodium and Potassium Intake in Healthy Adults in Thessaloniki Greater Metropolitan Area—The Salt Intake in Northern Greece (SING) Study
by Eleni Vasara, Georgios Marakis, Joao Breda, Petros Skepastianos, Maria Hassapidou, Anthony Kafatos, Nikolaos Rodopaios, Alexandra A. Koulouri and Francesco P. Cappuccio
Nutrients 2017, 9(4), 417; https://doi.org/10.3390/nu9040417 - 22 Apr 2017
Cited by 34 | Viewed by 7365
Abstract
A reduction in population sodium (as salt) consumption is a global health priority, as well as one of the most cost-effective strategies to reduce the burden of cardiovascular disease. High potassium intake is also recommended to reduce cardiovascular disease. To establish effective policies [...] Read more.
A reduction in population sodium (as salt) consumption is a global health priority, as well as one of the most cost-effective strategies to reduce the burden of cardiovascular disease. High potassium intake is also recommended to reduce cardiovascular disease. To establish effective policies for setting targets and monitoring effectiveness within each country, the current level of consumption should be known. Greece lacks data on actual sodium and potassium intake. The aim of the present study was therefore to assess dietary salt (using sodium as biomarker) and potassium intakes in a sample of healthy adults in northern Greece, and to determine whether adherence to a Mediterranean diet is related to different sodium intakes or sodium-to-potassium ratio. A cross-sectional survey was carried out in the Thessaloniki greater metropolitan area (northern Greece) (n = 252, aged 18–75 years, 45.2% males). Participants’ dietary sodium and potassium intakes were determined by 24-hour urinary sodium and potassium excretions. In addition, we estimated their adherence to Mediterranean diet by the use of an 11-item MedDietScore (range 0–55). The mean sodium excretion was 175 (SD 72) mmol/day, equivalent to 4220 (1745) mg of sodium or 10.7 (4.4) g of salt per day, and the potassium excretion was 65 (25) mmol/day, equivalent to 3303 (1247) mg per day. Men had higher sodium and potassium excretions compared to women. Only 5.6% of the sample had salt intake <5 g/day, which is the target intake recommended by the World Health Organization. Mean sodium-to-potassium excretion ratio was 2.82 (1.07). There was no significant difference in salt or potassium intake or their ratio across MedDietScore quartiles. No significant relationships were found between salt intake and adherence to a Mediterranean diet, suggesting that the perception of the health benefits of the Mediterranean diet does not hold when referring to salt consumption. These results suggest the need for a larger, nation-wide survey on salt intake in Greece and underline the importance of continuation of salt reduction initiatives in Greece. Full article
(This article belongs to the Special Issue Reducing Dietary Sodium and Improving Human Health)
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<p>Distribution of single 24-hour salt intake estimates (see text for conversion of urinary excretions to estimates intakes).</p>
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<p>Distribution of dietary sodium-to-potassium ratios (mg/mg) in the sample of 24-hour intake estimates (see text for conversion of urinary excretions to estimates intakes).</p>
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Review
Association of Polyphenol Biomarkers with Cardiovascular Disease and Mortality Risk: A Systematic Review and Meta-Analysis of Observational Studies
by Johanna Rienks, Janett Barbaresko and Ute Nöthlings
Nutrients 2017, 9(4), 415; https://doi.org/10.3390/nu9040415 - 22 Apr 2017
Cited by 86 | Viewed by 8770
Abstract
Epidemiologic studies have suggested an inverse association between flavonoids and cardiovascular disease (CVD). However, the results might have been influenced by the use of dietary assessment methods, which are error prone. The aim of this paper was to systematically review and analyse the [...] Read more.
Epidemiologic studies have suggested an inverse association between flavonoids and cardiovascular disease (CVD). However, the results might have been influenced by the use of dietary assessment methods, which are error prone. The aim of this paper was to systematically review and analyse the literature for evidence of associations between polyphenol biomarkers and CVD and mortality risk in observational studies. Eligible studies were identified through PubMed, Web of Science, and reference lists. Multivariable adjusted associations were extracted. Data were log-transformed and pooled using the random effects model. In total, eight studies were included, investigating 16 different polyphenol biomarkers in association with CVD and mortality. Blood and urine were used as biospecimens, and enterolactone, a lignan metabolite, was most often investigated. Three meta-analyses were conducted investigating the association between enterolactone, and all-cause and CVD mortality, and non-fatal myocardial infarction. A 30% and 45% reduced all-cause and CVD mortality risk were revealed at higher enterolactone concentrations. Furthermore, inverse associations were observed between polyphenol biomarkers and all-cause mortality, kaempferol, and acute coronary syndrome. There is evidence to suggest that enterolactone is associated with a lower CVD mortality risk. This emphasises the importance of the role of the microbiota in disease prevention. To strengthen the evidence, more studies are warranted. Full article
(This article belongs to the Special Issue Effects of Polyphenol-Rich Foods on Human Health)
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<p>Flowchart of the study selection.</p>
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<p>Forest of the association between enterolactone and (<b>a</b>) all-cause mortality; (<b>b</b>) CVD-mortality; and (<b>c</b>) non-fatal MI.</p>
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Article
Suppression of Oxidative Stress and NFκB/MAPK Signaling by Lyophilized Black Raspberries for Esophageal Cancer Prevention in Rats
by Ni Shi, Fang Chen, Xiaoli Zhang, Steven K. Clinton, Xiaofei Tang, Zheng Sun and Tong Chen
Nutrients 2017, 9(4), 413; https://doi.org/10.3390/nu9040413 - 22 Apr 2017
Cited by 35 | Viewed by 5845
Abstract
Research in the laboratory has shown that lyophilized black raspberries (BRB) significantly inhibit N-nitrosomethylbenzylamine (NMBA)-induced esophageal squamous cell carcinogenesis in rats. The objective of the present study is to characterize the underlying mechanism(s) of anti-cancer action of BRB in this preclinical animal [...] Read more.
Research in the laboratory has shown that lyophilized black raspberries (BRB) significantly inhibit N-nitrosomethylbenzylamine (NMBA)-induced esophageal squamous cell carcinogenesis in rats. The objective of the present study is to characterize the underlying mechanism(s) of anti-cancer action of BRB in this preclinical animal model focusing on oxidative stress and its related oncogenic signaling pathways. Esophageal epithelial tissues were collected and assessed for markers of oxidative stress and nuclear factor κB (NFκB) and mitogen-activated protein kinase (MAPK). BRB reduced the incidence of esophageal cancer from 100% in NMBA-treated rats to 81.5% in rats treated with NMBA plus BRB (p < 0.05). Tumor multiplicity was reduced from 4.73 ± 0.45 tumors per esophagus in NMBA-treated rats to 1.44 ± 0.26 in rats treated with NMBA plus BRB (p < 0.001). The data indicated that NMBA treatment increased production of hydrogen peroxide and lipid hydroperoxide, reduced expression and activity of glutathione peroxidase and superoxide dismutase 2, and activated NFκB/MAPK signaling in rat esophagus. The study’s results show that BRB reverses oxidative stress and suppresses NFκB/MAPK pathways, which could be the mechanisms for esophageal cancer chemopreventive action of BRB in rats. Full article
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<p>Black raspberries (BRB) decreases level of 8-OxoG. (<b>A</b>) Immunohistochemistry (IHC) staining of 8-OxoG in normal animals and rats treated with <span class="html-italic">N</span>-nitrosomethylbenzylamine (NMBA) or NMBA + BRB (200×). The upper right image is the version under 100×; and (<b>B</b>) statistical analysis of 8-OxoG staining. The values are expressed as mean; bars, ±SE. * <span class="html-italic">p</span> &lt; 0.05.</p>
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<p>BRB increases expression levels of glutathione peroxidase (GPx) and superoxide dismutase 2 (SOD2). (<b>A</b>,<b>B</b>), mRNA expression of GPx and SOD2 in rat esophagus; (<b>C</b>,<b>D</b>), protein expression of GPx and SOD2 in rat esophagus. The values are expressed as mean; bars, ±SE. ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001; **** <span class="html-italic">p</span> &lt; 0.0001.</p>
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<p>BRB suppressed activation of nuclear factor κB (NFκB) and mitogen-activated protein kinase (MAPK) signaling. (<b>A</b>) Western blot detected phosphorylation of extracellular signal–regulated kinases (ERK), p38 MAPK, stress-activated protein kinase/Jun amino-terminal kinases (SAPK/JNK), NFκB-p65, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα), and IκB kinase alpha/beta (IKK)α/β in rat esophagus; and (<b>B</b>) quantitative analysis of western blot. The values are expressed as mean; bars, ±SE. **** <span class="html-italic">p</span> &lt; 0.0001.</p>
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<p>Correlations between H<sub>2</sub>O<sub>2</sub> production and phosphorylation of NFκB p65 (<b>A</b>) or p38 MAPK (<b>B</b>) in NMBA-treated rat esophagus.</p>
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<p>Possible mechanisms of action of BRB in esophageal cancer prevention. Upper figure, BRB modulates oxidative stress/antioxidant pathway; lower figure, BRB inhibits MAPK and NFκB activation. Arrows indicate activation and T-lines indicate inhibition. L-Arg: L-arginine; iNOS: inducible nitric oxide synthase; ONOO: Peroxynitrite; GSSG: glutathione disulfide; NADPH: nicotinamide adenine dinucleotide phosphate reduced form; GSH: hydroperoxides using glutathione; GR: glutathione reductase; ROS/RNS: reactive oxygen species and reactive nitrogen species; P: phosphorylation; MEK: mitogen-activated protein kinase kinase; MKK: mitogen-activated protein kinase kinase; Erk: extracellular-signal-regulated kinases; COX-2: cyclooxygenase 2; PGE<sub>2</sub>: prostaglandin E2.</p>
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Article
The Association of Ankle Brachial Index, Protein-Energy Wasting, and Inflammation Status with Cardiovascular Mortality in Patients on Chronic Hemodialysis
by Hideki Ishii, Hiroshi Takahashi, Yasuhiko Ito, Toru Aoyama, Daisuke Kamoi, Takashi Sakakibara, Norio Umemoto, Yoshitaka Kumada, Susumu Suzuki and Toyoaki Murohara
Nutrients 2017, 9(4), 416; https://doi.org/10.3390/nu9040416 - 21 Apr 2017
Cited by 37 | Viewed by 5756
Abstract
Protein-energy wasting (PEW) is highly prevalent in hemodialysis (HD) patients. We investigated the association of abnormal ankle brachial index (ABI), PEW, and chronic inflammation status with clinical prognosis in HD patients. A total of 973 HD patients were enrolled and were followed-up for [...] Read more.
Protein-energy wasting (PEW) is highly prevalent in hemodialysis (HD) patients. We investigated the association of abnormal ankle brachial index (ABI), PEW, and chronic inflammation status with clinical prognosis in HD patients. A total of 973 HD patients were enrolled and were followed-up for 8 years. As a marker of the PEW, geriatric nutritional risk index (GNRI) was used. Cut-off levels were 91.2 for GNRI defined from previous studies and 1.9 mg/L for C-reactive protein (CRP) as median value, respectively. Abnormal ABI was seen in 332 (34.1%) patients. Declined GNRI and elevated CRP levels were independently associated with abnormal ABI (odds ratio (OR) 0.97, 95% confidence interval (CI) 0.96–0.99, p = 0.0009 and OR 1.40, 95% CI 1.07–1.83, p = 0.013, respectively). GNRI levels were also independently correlated with CRP levels (β = −0.126, p < 0.0001). During follow-up period, 283 (29.1%) patients died, including 123 (12.6%) due to cardiovascular disease (CVD). Abnormal ABI (adjusted hazard ratio (HR) 1.62, 95% CI 1.13–2.32, p = 0.0096), GNRI < 91.2 (adjusted HR 1.57, 95% CI 1.06–2.33, p = 0.023) and CRP > 1.9 mg/L (adjusted HR 1.89, 95% CI 1.31–2.77, p = 0.0007) independently predicted mortality due to CVD, respectively. In conclusion, abnormal ABI, GNRI, and CRP levels were closely associated with each other, and the combination of these variables increase their predictive values for the risk of mortality due to CVD and all-cause mortality in HD patients. Full article
(This article belongs to the Special Issue Nutrition and Chronic Kidney Disease)
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<p>Cardiovascular survival among groups according to number of risk factors, abnormal ABI, GNRI, and CRP.</p>
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<p>All-cause survival among groups according to number of risk factors, abnormal ABI, GNRI, and CRP.</p>
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Article
Curcumin Inhibits Apoptosis of Chondrocytes through Activation ERK1/2 Signaling Pathways Induced Autophagy
by Xiaodong Li, Kai Feng, Jiang Li, Degang Yu, Qiming Fan, Tingting Tang, Xiao Yao and Xiaoqing Wang
Nutrients 2017, 9(4), 414; https://doi.org/10.3390/nu9040414 - 21 Apr 2017
Cited by 105 | Viewed by 11208
Abstract
Osteoarthritis (OA) is an inflammatory disease of load-bearing synovial joints that is currently treated with drugs that exhibit numerous side effects and are only temporarily effective in treating pain, the main symptom of the disease. Consequently, there is an acute need for novel, [...] Read more.
Osteoarthritis (OA) is an inflammatory disease of load-bearing synovial joints that is currently treated with drugs that exhibit numerous side effects and are only temporarily effective in treating pain, the main symptom of the disease. Consequently, there is an acute need for novel, safe, and more effective chemotherapeutic agents for the treatment of osteoarthritis and related arthritic diseases. Curcumin, the principal curcuminoid and the most active component in turmeric, is a biologically active phytochemical. Evidence from several recent in vitro studies suggests that curcumin may exert a chondroprotective effect through actions such as anti-inflammatory, anti-oxidative stress, and anti-catabolic activity that are critical for mitigating OA disease pathogenesis and symptoms. In the present study, we investigated the protective mechanisms of curcumin on interleukin 1β (IL-1β)-stimulated primary chondrocytes in vitro. The treatment of interleukin (IL)-1β significantly reduces the cell viability of chondrocytes in dose and time dependent manners. Co-treatment of curcumin with IL-1β significantly decreased the growth inhibition. We observed that curcumin inhibited IL-1β-induced apoptosis and caspase-3 activation in chondrocytes. Curcumin can increase the expression of phosphorylated extracellular signal-regulated kinases 1/2 (ERK1/2), autophagy marker light chain 3 (LC3)-II, and Beclin-1 in chondrocytes. The expression of autophagy markers could be decreased when the chondrocytes were incubated with ERK1/2 inhibitor U0126. Our results suggest that curcumin suppresses apoptosis and inflammatory signaling through its actions on the ERK1/2-induced autophagy in chondrocytes. We propose that curcumin should be explored further for the prophylactic treatment of osteoarthritis in humans and companion animals. Full article
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<p>Chemical structures of curcumin. Curcumin is derived from the rhizomes of turmeric (<span class="html-italic">Curcuma longa</span>).</p>
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<p>Effects of curcumin and interleukin 1β (IL-1β) on the viability and proliferation of primary chondrocytes in vitro. To evaluate the effect of curcumin or IL-1β-induced cytotoxicity, primary chondrocytes were treated with 10 ng/mL, 15 ng/mL, 20 ng/mL, and 25 ng/mL IL-1β or 5 μM/L, 10 μM/L, 15 μM/L, and 20 μM/L curcumin for the following times: 6 h (<b>A</b>), 12 h (<b>B</b>), 24 h (<b>C</b>), and 48 h (<b>D</b>). IL-1β has a significant cytotoxic effect on chondrocytes. Results are expressed as means ± SD for experiments performed in triplicate. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001 compared with controls. (<b>E</b>) Immunofluorescence identification of collagen II (red) in primary chondrocytes.</p>
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<p>Effects of curcumin on IL-1β-induced apoptosis in primary chondrocytes. (<b>A</b>) Apoptotic cells were visualized using terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) fluorescence immunocytochemistry (green). Nuclei were counterstained with 4′,6-diamidino-2-phenylindole (DAPI) (blue); (<b>C</b>) Flow cytometric detection of apoptosis in the chondrocytes. Apoptotic cells labeled with Annexin V and propidium iodide (PI) fluorescence were estimated by flow cytometry. The percentages of cells in each quadrant is indicative of: upper left, necrotic cells; lower left, live cells; lower right, early apoptotic cells; and upper right, late apoptotic cells; (<b>D</b>) Accumulation of cleaved caspase 3 and bcl-2 was visualized by western blot. Results shown in (<b>B</b>,<b>E</b>,<b>F</b>) are expressed as means ± SD for experiments performed in triplicate. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001.Con, control; Rap, rapamycin; Cur, curcumin; 3-MA, 3-Methyladenine.</p>
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<p>Curcumin activated autophagy within chondrocytes. The curcumin induced autophagy was detected by monodansylcadaverine (MDC) staining ((<b>A</b>), quantified in (<b>B</b>)) and transmission electron microscope (TEM) (<b>C</b>) at 24 h. Accumulation of autophagosomes was observed in chondrocytes that were pretreated with curcumin (<b>C</b>). Accumulation of beclin1 and light chain 3 (LC3)-II upon autophagy activation was visualized by western blot ((<b>D</b>), quantified in (<b>E</b>) and (<b>F</b>)). Results in (<b>B</b>,<b>E</b>,<b>F</b>) are expressed as means ± SD for experiments performed in triplicate. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001. Cur, curcumin; Rap, rapamycin; 3-MA, 3-Methyladenine.</p>
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<p>Curcumin reverses U0126-induced inhibition of extracellular signal-regulated kinases 1/2(ERK1/2) in primary chondrocytes. (<b>A</b>) p-ERK was visualized by western blot in U0126-treated chondrocytes. Serum-starved chondrocytes were preincubated with 10 μm curcumin for indicated time points and co-treated with 10 μm U0126 for 10 min, 20 min, 30 min, and 60 min. Curcumin pretreatment reversed U0126-induced ERK1/2 inhibition in a time-dependent manner. The pan ERK1/2 was not affected (and quantified in (<b>B</b>)). (<b>C</b>) Effects of curcumin on IL-1β-induced inhibition of mitogen-activated protein kinase (MAPK)/ERK1/2 pathway in primary chondrocytes in vitro. Serum-starved chondrocytes were pre-stimulated with 10 μm curcumin alone for 4 h and then co-treated with IL-1β (10 ng/mL) and/or 10 μm U0126 for 24 h. Some cultures were left untreated and evaluated after 24 h. Results in (<b>B</b>,<b>D</b>) are expressed as means ± SD for experiments performed in triplicate. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001. Cur, curcumin.</p>
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<p>Curcumin could activate autophagy for U0126-induced inhibition of ERK1/2 in primary chondrocytes. Accumulation of beclin-1 and LC3-II upon autophagy activation was visualized by western blot ((<b>A</b>), quantified in (<b>B</b>) and (<b>C</b>)). Results in (<b>B</b>,<b>C</b>) are expressed as means ± SD for experiments performed in triplicate.* <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001. Rap, rapamycin; 3-MA, 3-Methyladenine.</p>
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<p>Curcumin induced autophagy via the ERK1/2 signal pathway to protect chondrocytes from apoptosis. IL-1β stimulates the IL-1β receptor, initiating an intracellular signal transduction cascade, which inhibits the cytoplasmic MAPK/ERK1/2 signaling pathway, then activates proinflammatory and pro-apoptotic gene production. ERK1/ERK2, a downstream kinase of the MAPK pathway, regulates the expression and activity of various transcription factors. Specific inhibition of ERK1/ERK2 by U0126 or IL-1β results in cleavage of caspase-3 in primary chondrocytes in vitro. Since activation of caspase-3 and DNA fragmentation are common features of apoptosis, the specific inhibition of the Ras-mitogen-activated kinase leads to chondrocyte apoptosis. Curcumin blocks the inhibition effect of U0126 or IL-1β on the MAPK pathway and activates autophagy in chondrocytes. Beclin-1 promotes LC3 activation. Recruitment and integration of LC3B-II into the growing phagophore, eventually results in the formation of autophagosomes.</p>
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Concept Paper
“Eat as If You Could Save the Planet and Win!” Sustainability Integration into Nutrition for Exercise and Sport
by Nanna Meyer and Alba Reguant-Closa
Nutrients 2017, 9(4), 412; https://doi.org/10.3390/nu9040412 - 21 Apr 2017
Cited by 46 | Viewed by 20971
Abstract
Today’s industrial food production contributes significantly to environmental degradation. Meat production accounts for the largest impact, including greenhouse gas emissions, land and water use. While food production and consumption are important aspects when addressing climate change, this article focuses predominantly on dietary change [...] Read more.
Today’s industrial food production contributes significantly to environmental degradation. Meat production accounts for the largest impact, including greenhouse gas emissions, land and water use. While food production and consumption are important aspects when addressing climate change, this article focuses predominantly on dietary change that promotes both health for planet and people with focus on athletes. Healthy, sustainable eating recommendations begin to appear in various governmental guidelines. However, there remains resistance to the suggested reductions in meat consumption. While food citizens are likely to choose what is good for them and the planet, others may not, unless healthy eating initiatives integrate creative food literacy approaches with experiential learning as a potential vehicle for change. This concept paper is organized in three sections: (1) Environmental impact of food; (2) health and sustainability connections; and (3) application in sports and exercise. For active individuals, this article focuses on the quantity of protein, highlighting meat and dairy, and quality of food, with topics such as organic production and biodiversity. Finally, the timing of when to integrate sustainability principles in sport nutrition is discussed, followed by practical applications for education and inclusion in team, institutional, and event operations. Full article
(This article belongs to the Special Issue Nutrition, Health and Athletic Performance)
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Article
Testing the Capacity of a Multi-Nutrient Profiling System to Guide Food and Beverage Reformulation: Results from Five National Food Composition Databases
by Emilie Combet, Antonis Vlassopoulos, Famke Mölenberg, Mathilde Gressier, Lisa Privet, Craig Wratten, Sahar Sharif, Florent Vieux, Undine Lehmann and Gabriel Masset
Nutrients 2017, 9(4), 406; https://doi.org/10.3390/nu9040406 - 21 Apr 2017
Cited by 15 | Viewed by 9065
Abstract
Nutrient profiling ranks foods based on their nutrient composition, with applications in multiple aspects of food policy. We tested the capacity of a category-specific model developed for product reformulation to improve the average nutrient content of foods, using five national food composition datasets [...] Read more.
Nutrient profiling ranks foods based on their nutrient composition, with applications in multiple aspects of food policy. We tested the capacity of a category-specific model developed for product reformulation to improve the average nutrient content of foods, using five national food composition datasets (UK, US, China, Brazil, France). Products (n = 7183) were split into 35 categories based on the Nestlé Nutritional Profiling Systems (NNPS) and were then classified as NNPS ‘Pass’ if all nutrient targets were met (energy (E), total fat (TF), saturated fat (SFA), sodium (Na), added sugars (AS), protein, calcium). In a modelling scenario, all NNPS Fail products were ‘reformulated’ to meet NNPS standards. Overall, a third (36%) of all products achieved the NNPS standard/pass (inter-country and inter-category range: 32%–40%; 5%–72%, respectively), with most products requiring reformulation in two or more nutrients. The most common nutrients to require reformulation were SFA (22%–44%) and TF (23%–42%). Modelled compliance with NNPS standards could reduce the average content of SFA, Na and AS (10%, 8% and 6%, respectively) at the food supply level. Despite the good potential to stimulate reformulation across the five countries, the study highlights the need for better data quality and granularity of food composition databases. Full article
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<p>Overall pass rate (proportion of products meeting the Nestlé Nutritional Profiling System criteria) across all databases.</p>
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<p>Pass rate for the 11 major categories (proportion of products meeting the NNPS criteria) across all databases (weighted average, min, max).</p>
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<p>Average minimum change (%) required in NNPS fail products to achieve NNPS standards (circle), and overall modelled change (%) in all products amenable to reformulation (squares), across all five national datasets (weighted average, min, max). Circles: change required in NNPS Fail products for the specific nutrient; squares: overall change in the average nutrient content across all products analysed.</p>
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Article
Endurance Training with or without Glucose-Fructose Ingestion: Effects on Lactate Metabolism Assessed in a Randomized Clinical Trial on Sedentary Men
by Robin Rosset, Virgile Lecoultre, Léonie Egli, Jérémy Cros, Valentine Rey, Nathalie Stefanoni, Valérie Sauvinet, Martine Laville, Philippe Schneiter and Luc Tappy
Nutrients 2017, 9(4), 411; https://doi.org/10.3390/nu9040411 - 20 Apr 2017
Cited by 7 | Viewed by 6553
Abstract
Glucose-fructose ingestion increases glucose and lactate oxidation during exercise. We hypothesized that training with glucose-fructose would induce key adaptations in lactate metabolism. Two groups of eight sedentary males were endurance-trained for three weeks while ingesting either glucose-fructose (GF) or water (C). Effects of [...] Read more.
Glucose-fructose ingestion increases glucose and lactate oxidation during exercise. We hypothesized that training with glucose-fructose would induce key adaptations in lactate metabolism. Two groups of eight sedentary males were endurance-trained for three weeks while ingesting either glucose-fructose (GF) or water (C). Effects of glucose-fructose on lactate appearance, oxidation, and clearance were measured at rest and during exercise, pre-training, and post-training. Pre-training, resting lactate appearance was 3.6 ± 0.5 vs. 3.6 ± 0.4 mg·kg−1·min−1 in GF and C, and was increased to 11.2 ± 1.4 vs. 8.8 ± 0.7 mg·kg−1·min−1 by exercise (Exercise: p < 0.01). Lactate oxidation represented 20.6% ± 1.0% and 17.5% ± 1.7% of lactate appearance at rest, and 86.3% ± 3.8% and 86.8% ± 6.6% during exercise (Exercise: p < 0.01) in GF and C, respectively. Training with GF increased resting lactate appearance and oxidation (Training × Intervention: both p < 0.05), but not during exercise (Training × Intervention: both p > 0.05). Training with GF and C had similar effects to increase lactate clearance during exercise (+15.5 ± 9.2 and +10.1 ± 5.9 mL·kg−1·min−1; Training: p < 0.01; Training × Intervention: p = 0.97). The findings of this study show that in sedentary participants, glucose-fructose ingestion leads to high systemic lactate appearance, most of which is disposed non-oxidatively at rest and is oxidized during exercise. Training with or without glucose-fructose increases lactate clearance, without altering lactate appearance and oxidation during exercise. Full article
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<p>Study design (<b>a</b>) and description of the metabolic evaluations (<b>b</b>). Drinks containing 19 g glucose and 12 g fructose were administered at time 0, 30 and 60 min at rest, and at 20 min intervals during exercise. Primed-continuous infusions of (6,6-<sup>2</sup>H<sub>2</sub>)-<span class="html-small-caps">d</span>-(+)-glucose and Na-(3-<sup>13</sup>C<sub>1</sub>)-<span class="html-small-caps">l</span>-(+)-lactate were started at time 0, and resting measurements were obtained after 60 min equilibration. Continuous infusion rates were upgraded at the beginning of exercise at time 100 min (see methods for further details). GF: intervention in which glucose-fructose drinks were provided during training sessions; C: control intervention in which plain water was provided during training sessions.</p>
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<p>Changes over time of earlobe blood lactate concentration in GF and C groups during training sessions. GF received glucose-fructose drinks and C received water −20, 0, and +20 min relative to exercise onset. Effects of exercise (E) and intervention (I) were compared using a mixed-model analysis. Paired and unpaired contrasts were used to determine differences between rest and exercise (E effect: time = 0 min vs. time = 30–60 min: <span>$</span>: <span class="html-italic">p</span> &lt; 0.01) and GF vs. C (I effect: *: <span class="html-italic">p</span> &lt; 0.05). Mean ± SEM for <span class="html-italic">n</span> = 8 participants in all groups.</p>
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<p>Changes over time of plasma (<b>a</b>) glucose, (<b>b</b>) lactate and (<b>c</b>) fructose concentrations in GF (<b>left</b>) and C (<b>right</b>) participants during metabolic evaluations. Glucose-fructose drinks were provided both at rest (time = 0–90 min) and during exercise (time = 100–190 min) in all tests. GF pre-training (GF Pre) and C pre-training (C Pre) is indicated in white, GF post-training (GF Post) in black and C post-training (C Post) in grey. Effects of exercise and interventions were compared using a mixed-model analysis. Paired contrasts were used for rest vs. exercise periods (E effect: <span>$</span>: <span class="html-italic">p</span> &lt; 0.01) and pre- vs. post-training (T effect: #: <span class="html-italic">p</span> &lt; 0.05; ##: <span class="html-italic">p</span> &lt; 0.01). Dashed zones: Measures considered for tracer calculations. Mean ± SEM for <span class="html-italic">n</span> = 8 participants in all groups.</p>
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<p>Changes over time of plasma (<b>a</b>) (<sup>2</sup>H<sub>2</sub>)glucose, (<b>b</b>) (<sup>13</sup>C)glucose, (<b>c</b>) (<sup>13</sup>C<sub>1</sub>)lactate and (<b>d</b>) expired air <sup>13</sup>CO<sub>2</sub> isotopic enrichments in GF (<b>left</b>) and C (<b>right</b>) participants during metabolic evaluations. Glucose-fructose drinks were provided in all tests, both during rest (time = 0–90 min) and exercise (time = 100–190 min) periods. GF pre-training (GF Pre) and C pre-training (C Pre) is indicated in white, GF post-training (GF Post) in black and C post-training (C Post) in grey. Effects of exercise and training interventions were compared using a mixed-model analysis. Paired contrasts were used for rest vs. exercise periods (E effect: <span>$</span>: <span class="html-italic">p</span> &lt; 0.01) and training × interventions (T × I effect: *: <span class="html-italic">p</span> &lt; 0.05). Dashed zones: Measures considered for tracer calculations. Mean ± SEM for <span class="html-italic">n</span> = 8 participants in all groups.</p>
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Article
Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a High-Fat Diet: The Role of Irisin, Adiponectin and Proinflammatory Biomarkers
by Agnieszka Irena Mazur-Bialy, Jan Bilski, Dagmara Wojcik, Bartosz Brzozowski, Marcin Surmiak, Magdalena Hubalewska-Mazgaj, Anna Chmura, Marcin Magierowski, Katarzyna Magierowska, Tomasz Mach and Tomasz Brzozowski
Nutrients 2017, 9(4), 410; https://doi.org/10.3390/nu9040410 - 20 Apr 2017
Cited by 48 | Viewed by 9094
Abstract
Inflammatory bowel diseases (IBDs) are a heterogeneous group of disorders exhibited by two major phenotypic forms: Crohn‘s disease and ulcerative colitis. Although the aetiology of IBD is unknown, several factors coming from the adipose tissue and skeletal muscles, such as cytokines, adipokines and [...] Read more.
Inflammatory bowel diseases (IBDs) are a heterogeneous group of disorders exhibited by two major phenotypic forms: Crohn‘s disease and ulcerative colitis. Although the aetiology of IBD is unknown, several factors coming from the adipose tissue and skeletal muscles, such as cytokines, adipokines and myokines, were suggested in the pathogenesis of ulcerative colitis; however, it has not been extensively studied whether voluntary exercise can ameliorate that disorder. We explored the effect of moderate exercise (i.e., voluntary wheel running) on the disease activity index (DAI), colonic blood flow (CBF), plasma irisin and adiponectin levels and real-time PCR expression of proinflammatory markers in mesenteric fat in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS) colitis fed a high-fat diet (HFD) compared to those on a standard chow diet (SD). Macroscopic and microscopic colitis in sedentary SD mice was accompanied by a significant fall in CBF, some increase in colonic tissue weight and a significant increase in the plasma levels of tumour necrosis factor-alpha (TNF-α), IL-6, monocyte chemotactic protein 1 (MCP-1) and IL-13 (p < 0.05). In sedentary HFD mice, colonic lesions were aggravated, colonic tissue weight increased and the plasma TNF-α, IL-6, MCP-1, IL-1β and leptin levels significantly increased. Simultaneously, a significant decrease in the plasma irisin and adiponectin levels was observed in comparison with SD mice (p < 0.05). Exercise significantly decreased macroscopic and microscopic colitis, substantially increased CBF and attenuated the plasma TNF-α, IL-6, MCP-1, IL-1β and leptin levels while raising the plasma irisin and the plasma and WAT concentrations of adiponectin in HFD mice (p < 0.05). We conclude that: (1) experimental colitis is exacerbated in HFD mice, possibly due to a fall in colonic microcirculation and an increase in the plasma and mesenteric fat content of proinflammatory biomarkers; and (2) voluntary physical activity can attenuate the severity of colonic damage in mice fed a HFD through the release of protective irisin and restoration of plasma adiponectin. Full article
(This article belongs to the Special Issue Nutrition and Diet in IBD)
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<p>A flow chart presenting the experimental protocol and time duration of this study.</p>
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<p>Energy intake in the mice fed a SD or HFD with or without voluntary exercise. Results are mean ± standard error of the mean S.E.M. of eight animals per each group. An asterisk indicates a significant change as compared to the respective values in the sedentary mice fed a SD with or without voluntary exercise (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test).</p>
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<p>The running distance in the mice fed a SD or HFD and subjected to voluntary exercise. Note that the animals were initially fed a SD and HFD over the period of 12 weeks and subsequently subjected to voluntary exercise for a period of six weeks. Results are mean ± S.E.M. of eight animals per each group. An asterisk indicates a significant change as compared to the respective values in sedentary exercising mice fed a SD (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test).</p>
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<p>Body weight in grams and mesenteric fat pad per body weight (%) in sedentary (Seden) or voluntary exercising (Volunt) mice with or without TNBS-induced colitis fed a standard diet (SD) or a high-fat diet (HFD). Results are mean ± S.E.M. of eight animals per each group. An asterisk indicates a significant change as compared to the respective values in the sedentary mice with or without colitis fed a HFD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A cross indicates a significant change as compared to the respective values in the sedentary mice with colitis fed a HFD (<span class="html-italic">p</span> &lt; 0.05, ANOVA).</p>
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<p>The representative gross appearance of the colon obtained from: (<b>A</b>) a sedentary mouse without colitis fed a standard diet (SD); (<b>B</b>) a sedentary mouse with TNBS colitis fed a standard diet (SD); (<b>C</b>) a sedentary mouse with TNBS colitis fed a HFD without voluntary exercise; and (<b>E</b>) a mouse with TNBS colitis fed a HFD, subjected to voluntary exercise and sacrificed at day 4 after the induction of colitis. The photomicrographs represent: (<b>A</b>) a normal colon from a sedentary mouse without colitis fed a SD: normal macroscopic appearance of the colonic mucosa; (<b>B</b>) a colon from a sedentary mouse with colitis fed a SD: haemorrhagic lesions and a bloody effusion; (<b>C</b>) a colon from a sedentary mouse with colitis fed a HFD: more severe haemorrhagic lesions with a bloody effusion involving the entire intestine; (<b>D</b>) a colon from a sedentary mouse fed a SD with voluntary exercise: a less severe intestinal damage and bleeding; (<b>E</b>) a colon from a mouse fed a HFD with voluntary exercise: marked improvement in colitis as manifested by a reduction in bleeding, haemorrhagic lesions and macroscopic signs of mucosal injury.</p>
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<p>The representative microscopic appearance of the colonic mucosa in: a sedentary mouse without TNBS colitis fed a SD (<b>A</b>); a sedentary mouse with TNBS colitis fed a SD (<b>B</b>); one with colitis fed a SD and subjected to voluntary exercise (<b>C</b>); a sedentary mouse with colitis fed a HFD (<b>D</b>); a mouse with colitis fed a HFD and subjected to voluntary exercise (<b>E</b>). The colonic mucosa of the sedentary mouse (<b>A</b>) shows normal crypt architecture but inflammatory exudates and mucosal damage are observed in the sedentary mouse fed a SD and administered with TNBS (<b>B</b>); that inflammatory reaction is less intense and the mucosal damage is attenuated in the colonic mucosa of the TNBS mouse fed a SD and subjected to voluntary exercise (<b>C</b>). Colonic inflammation, neutrophil infiltration and a loss in the mucosal architecture are worsened in the sedentary mouse with colitis fed a HFD (<b>D</b>). In contrast, the microscopic appearance of colonic mucosa in the TNBS mouse fed a HFD and subjected to voluntary exercise showed a less severe inflammation and neutrophil infiltration, and attenuation of colonic damage with signs of regeneration as compared to the sedentary mouse with HFD (<b>E</b>).</p>
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<p>The effect of exercise on the disease activity index (DAI) and alterations in colonic blood flow (CBF) in sedentary (Seden) animals with TNBS-induced colitis fed a standard diet (SD) or a high-fat diet (HFD), with or without voluntary exercise (Volunt). Results are mean ± S.E.M. of eight animals per each group. An asterisk indicates a significant change as compared to the respective values in the colitis mice fed a SD (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test). A cross indicates a significant change as compared to the respective values obtained in the animals fed a HFD but not subjected to exercise (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test).</p>
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<p>The plasma levels of TNF-α, MCP-1, IL-6 and IL-13 in sedentary mice with colitis fed a standard diet (SD) or high-fat diet (HFD) with or without voluntary exercise (Volunt). Please note the inhibitory effect of voluntary exercise on the proinflammatory biomarkers observed in the HFD mice with colitis. Results are mean ± S.E.M. of eight mice per each group. An asterisk indicates a significant difference as compared to the control groups of animals without colitis (<span class="html-italic">p</span> &lt; 0.05, ANOVA). An asterisk and a cross indicate a significant difference as compared to the values obtained in rats fed a SD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A cross indicates a significant difference as compared to the values obtained in the sedentary mice without colitis fed a HFD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A double cross indicates a significant change as compared to the HFD mice without voluntary exercise (<span class="html-italic">p</span> &lt; 0.05, ANOVA).</p>
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<p>The effect of exercise on the plasma levels of IL-17, IL-1α, KC and IL-4 in the sedentary mice with colitis fed a standard diet (SD) or those with colitis fed a high-fat diet (HFD), with or without voluntary exercise. Please note the inhibitory effect of voluntary exercise on the proinflammatory biomarkers observed in the HFD mice with colitis. Results are mean ± S.E.M. of eight mice per group. An asterisk indicates a significant difference as compared to the control group of sedentary animals without colitis (<span class="html-italic">p</span> &lt; 0.05, ANOVA). An asterisk and cross indicate a significant difference as compared to the values obtained in the sedentary mice without colitis fed a SD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A cross indicates a significant difference as compared to the values obtained in the sedentary mice without colitis fed a HFD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A double cross indicates a significant change as compared to the values obtained in the colitis mice fed a HFD without voluntary exercise (<span class="html-italic">p</span> &lt; 0.05, ANOVA).</p>
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<p>The plasma irisin levels in the sedentary mice (Seden) with or without TNBS colitis fed a standard diet (SD) or a high-fat diet (HFD) and subjected or not subjected to voluntary exercise (Volunt). Please note that the plasma irisin concentration was significantly diminished in the sedentary mice fed a HFD and that effect was reversed in the HFD mice subjected to voluntary exercise. Results are mean ± S.E.M. of eight animals per each experimental group. An asterisk indicates a significant change as compared to the respective values in the sedentary mice without colitis fed a SD (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test). An asterisk and a cross indicate a significant change as compared to the respective values in the colitis animals fed a SD (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test). A cross indicates a significant change as compared to the value obtained in the sedentary animals with colitis fed a HFD without voluntary exercise (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test).</p>
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<p>The plasma adiponectin and leptin levels in the sedentary mice with or without TNBS colitis fed a standard diet (SD) or a high-fat diet (HFD) subjected or not subjected to voluntary exercise (Volunt). Results are mean ± S.E.M. of eight animals per each experimental group. An asterisk indicates a significant change as compared to the respective values in the sedentary mice without colitis fed a SD (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test). An asterisk and a cross indicate a significant change as compared to the respective values in the TNBS colitis mice fed a SD (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test). A cross indicates a significant change as compared to the values obtained in the sedentary animals with colitis fed a HFD without voluntary exercise (<span class="html-italic">p</span> &lt; 0.05, <span class="html-italic">t</span>-test).</p>
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<p>The effect of exercise on the real-time PCR expression of mRNA for TNF-α, IL-6 and MCP-1 in the mesenteric fat of sedentary mice with colitis fed a SD or HFD with or without voluntary exercise. Results are mean ± S.E.M. of eight animals per each experimental group. An asterisk indicates a significant change (<span class="html-italic">p</span> &lt; 0.05, ANOVA) as compared to the respective values in the sedentary mice fed a SD. An asterisk and a cross indicate a significant change (<span class="html-italic">p</span> &lt; 0.05, ANOVA) as compared to the respective values in the sedentary animals with colitis fed a SD. A cross indicates a significant change (<span class="html-italic">p</span> &lt; 0.05, ANOVA) as compared to the values obtained in the sedentary colitis mice fed a HFD without exercise. A double cross indicates a significant change (<span class="html-italic">p</span> &lt; 0.05, ANOVA) as compared to the values obtained in the group of sedentary HFD animals with colitis not subjected to voluntary exercise.</p>
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<p>The effect of exercise on the real-time PCR expression of adiponectin and leptin in the mesenteric fat of sedentary mice with or without TNBS colitis fed a SD or HFD and subjected or not subjected to voluntary exercise. Results are mean ± S.E.M. of eight animals per each experimental group. An asterisk indicates a significant change as compared to the respective values in the sedentary mice fed a SD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). An asterisk and a cross indicate a significant change as compared to the respective values in the animals with colitis fed a SD (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A cross indicates a significant change as compared to the values obtained in the sedentary mice fed a HFD without exercise (<span class="html-italic">p</span> &lt; 0.05, ANOVA). A double cross indicates a significant change as compared to the values obtained in the sedentary HFD animals with colitis not subjected to voluntary exercise (<span class="html-italic">p</span> &lt; 0.05, ANOVA).</p>
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Erratum
Erratum: Effect of Fibre Supplementation on Body Weight and Composition, Frequency of Eating and Dietary Choice in Overweight Individuals Nutrients 2017, 9, 149
by Vicky A. Solah, Deborah A. Kerr, Wendy J. Hunt, Stuart K. Johnson, Carol J. Boushey, Edward J. Delp, Xingqiong Meng, Roland J. Gahler, Anthony P. James, Aqif S. Mukhtar, Haelee K. Fenton and Simon Wood
Nutrients 2017, 9(4), 409; https://doi.org/10.3390/nu9040409 - 20 Apr 2017
Cited by 20 | Viewed by 4137
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Reply
Response to Comments by Vuksan V. et al., Nutrients 2017, 9, 398, Regarding an Article by Solah V.A. et al., Nutrients 2017, 9, 149
by Vicky A. Solah, Deborah A. Kerr, Wendy J. Hunt, Stuart K. Johnson, Carol J. Boushey, Edward J. Delp, Xingqiong Meng, Roland J. Gahler, Anthony P. James, Aqif S. Mukhtar, Haelee K. Fenton and Simon Wood
Nutrients 2017, 9(4), 408; https://doi.org/10.3390/nu9040408 - 20 Apr 2017
Viewed by 3494
Abstract
To the Editor: We have read the comments by Dr. Vuksan regarding our article entitled “Effect of Fibre Supplementation on Body Weight and Composition, Frequency of Eating and Dietary Choice in Overweight Individuals” as published in Nutrients in February 2017 [1].[...] Full article
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Article
Prenatal Exposure to a Maternal High-Fat Diet Affects Histone Modification of Cardiometabolic Genes in Newborn Rats
by Bijaya Upadhyaya, Tricia Larsen, Shivon Barwari, Eli J. Louwagie, Michelle L. Baack and Moul Dey
Nutrients 2017, 9(4), 407; https://doi.org/10.3390/nu9040407 - 20 Apr 2017
Cited by 27 | Viewed by 6739
Abstract
Infants born to women with diabetes or obesity are exposed to excess circulating fuels during fetal heart development and are at higher risk of cardiac diseases. We have previously shown that late-gestation diabetes, especially in conjunction with a maternal high-fat (HF) diet, impairs [...] Read more.
Infants born to women with diabetes or obesity are exposed to excess circulating fuels during fetal heart development and are at higher risk of cardiac diseases. We have previously shown that late-gestation diabetes, especially in conjunction with a maternal high-fat (HF) diet, impairs cardiac functions in rat-offspring. This study investigated changes in genome-wide histone modifications in newborn hearts from rat-pups exposed to maternal diabetes and HF-diet. Chromatin-immunoprecipitation-sequencing revealed a differential peak distribution on gene promoters in exposed pups with respect to acetylation of lysines 9 and 14 and to trimethylation of lysines 4 and 27 in histone H3 (all, false discovery rate, FDR < 0.1). In the HF-diet exposed offspring, 54% of the annotated genes showed the gene-activating mark trimethylated lysine 4. Many of these genes (1) are associated with the “metabolic process” in general and particularly with “positive regulation of cholesterol biosynthesis” (FDR = 0.03); (2) overlap with 455 quantitative trait loci for blood pressure, body weight, serum cholesterol (all, FDR < 0.1); and (3) are linked to cardiac disease susceptibility/progression, based on disease ontology analyses and scientific literature. These results indicate that maternal HF-diet changes the cardiac histone signature in offspring suggesting a fuel-mediated epigenetic reprogramming of cardiac tissue in utero. Full article
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<p>Study timeline. Female rats were randomized into four groups. Two groups were fed high fat diet (HF) and two control diet (CD) for 28 days prior to their breeding and throughout the pregnancy. On gestational day 14, one each of HF and CD group received intraperitoneal injection of Streptozotocin (STZ, 65 mg/kg) and the remaining two received citrate buffer (CB) as a control. Pups were normally delivered on gestational day 22 and sacrificed for heart collection.</p>
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<p>Physiological characteristics of pups and corresponding mothers. Higher neonatal heart weight (<b>a</b>) and neonatal heart to body weight ratio (<b>b</b>) that correspond to elevated maternal late gestation glucose levels (<b>c</b>) in diabetes exposed group; <span class="html-italic">n</span> = 10–12 (<b>a</b>,<b>b</b>), <span class="html-italic">n</span> = 2 (<b>c</b>). * <span class="html-italic">p</span> &lt; 0.05, CC, controls; CS, diabetes exposed; HC, HF-diet exposed; HS, combination exposed.</p>
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<p>Differential histone modifications. Principal component analyses showing different profiles among three histone modifications (H3Ac, H3K4me3, and H3K27me3) and the four exposure groups. Axes showing % of variations. CC, controls; CS, diabetes exposed; HC, HF-diet exposed; HS, combination exposed.</p>
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<p>High fat and diabetes-induced genome wide differential histone marks. Heat maps showing read density along with corresponding mean density (tag/50 bp) plots in ±5 kb of any known transcriptional start site for H3Ac, H3K4me3, and H3K27me3 modifications clustered and visualized as four panels in the order of CC (control), CS (diabetes exposed), HC (diet exposed), and HS (combination exposed) from left to right. From the vertical view, clusters with the central density profile are located at the top, followed by clusters with peaks in the −5 kb region (marked within the black lines), those with peaks in the +5 kb region, those with diffuse read density, and those without significant read density.</p>
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<p>Enriched histone modification peaks overlapping 5 kb upstream region of known transcriptional start site. All H3Ac (Ac), H3K4me3 (K4), and H3K27me3 (K27) enriched peaks detected on the rat genome are shown for each exposure group. CC, controls; CS, diabetes exposed; HC, HF-diet exposed; HS, combination exposed.</p>
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<p>Gene ontology classification of genes with H3K4me3 enrichment histone modification due to high fat exposure. A representative gene ontology analysis of candidate genes corresponding to H3K4me3 peak enrichment in the diet exposed group (HC) is shown. Gene ontology of ‘metabolic process’ is chosen for the downstream analyses.</p>
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<p>Gene expression validation of selected candidate genes with enriched H3K4me3 marks (compared to controls) on their promoters. Beta-2-microglobulin was used as a reference gene for normalizing gene expression levels. <span class="html-italic">n</span> = 4, * <span class="html-italic">p</span> &lt; 0.05.</p>
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<p>Peaks detection in ChIP sequencing: Representative genomic region of a negative strand (chromosome 7) near the transcriptional start site of Atp5g2 gene, illustrating 5 kb upstream peaks in cyan (acetylation), red (H3K427me3), blue (H3K4me3), and grey (Input control) colors. CC, controls; CS, diabetes exposed; HC, HF-diet exposed; HS, HF-diet and diabetes exposed or combination exposed.</p>
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<p>Genome wide differential histone marks in H3Ac, H3K4me3, and H3K27me3 modifications. Read density in ±5 kb of any known transcriptional start site for each marker are clustered and visualized in a heat map that consists of three panels in the order of Ac, K27, and K4 (from left to right). A selected cluster with differential density profile centralized at the transcription start sites are marked under the blue lines, which shows a slight correlation (Pearson coefficient, <span class="html-italic">r</span> = 0.29) between K4 and Ac modifications while no correlation (Pearson coefficient, <span class="html-italic">r</span> = 0.09) is observed between K4 and K27 modifications due to maternal high fat( HF) diet. HC, HF-diet exposed treatment.</p>
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<p>Genic distributions of differential histone marks. (<b>a</b>) H3Ac, (<b>b</b>) H3K4me3, and (<b>c</b>) H3K27me3 in four diet groups around the TSS in four diet groups are plotted. Distances to the nearest TSS for peaks identified and plotted in pie charts. CC, controls; CS, diabetes exposed; HC, HF-diet-exposed; HS, diet and diabetes exposed or combination exposed; TSS: transcription start site; US: upstream; DS: downstream; IF: include feature; I: inside; OE: overlap end; OS: overlap start.</p>
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Review
Fructose Consumption in the Development of Obesity and the Effects of Different Protocols of Physical Exercise on the Hepatic Metabolism
by Rodrigo Martins Pereira, José Diego Botezelli, Kellen Cristina Da Cruz Rodrigues, Rania A. Mekary, Dennys Esper Cintra, José Rodrigo Pauli, Adelino Sanchez Ramos Da Silva, Eduardo Rochete Ropelle and Leandro Pereira De Moura
Nutrients 2017, 9(4), 405; https://doi.org/10.3390/nu9040405 - 20 Apr 2017
Cited by 92 | Viewed by 16002
Abstract
Fructose consumption has been growing exponentially and, concomitant with this, the increase in the incidence of obesity and associated complications has followed the same behavior. Studies indicate that fructose may be a carbohydrate with greater obesogenic potential than other sugars. In this context, [...] Read more.
Fructose consumption has been growing exponentially and, concomitant with this, the increase in the incidence of obesity and associated complications has followed the same behavior. Studies indicate that fructose may be a carbohydrate with greater obesogenic potential than other sugars. In this context, the liver seems to be a key organ for understanding the deleterious health effects promoted by fructose consumption. Fructose promotes complications in glucose metabolism, accumulation of triacylglycerol in the hepatocytes, and alterations in the lipid profile, which, associated with an inflammatory response and alterations in the redox state, will imply a systemic picture of insulin resistance. However, physical exercise has been indicated for the treatment of several chronic diseases. In this review, we show how each exercise protocol (aerobic, strength, or a combination of both) promote improvements in the obesogenic state created by fructose consumption as an improvement in the serum and liver lipid profile (high-density lipoprotein (HDL) increase and decrease triglyceride (TG) and low-density lipoprotein (LDL) levels) and a reduction of markers of inflammation caused by an excess of fructose. Therefore, it is concluded that the practice of aerobic physical exercise, strength training, or a combination of both is essential for attenuating the complications developed by the consumption of fructose. Full article
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<p>Role of fructose on metabolic diseases. Fructose reduces the phosphate biodisponibility, leading to acid uric production and nitric oxide synthase inhibition contributing to hypertension. Reduced phosphate biodisponibility also activates SIRT-Dependent deacetylase of FoxO1 contributing to gluconeogenesis and hyperglycemia. Fructose-1P upregulates PGC-1β expression by promoting lipogenesis through SREBP1c activation. The same nutrient provides carbon chains for the synthesis of triglycerides, diacilglycerides, and VLDL cholesterol contributing to hypertriglyceridemia, hepatic insulin resistance, and dyslipidemia. Sub products of fructose target other tissues, leading to systemic insulin resistance and inflammation. Finally, ROS generated by fructosylation increases oxidative damage and stress response in the inner of cell, leading to DNA damage and proinflammatory cytokines production. ACC: acetyil-coA carboxylase; ACC: Acetyl-CoA Carboxylase; ADP: Adenosine Diphosphate; AP-1: Activator Protein-1; ATP: Adenosine Triphosphate; CPT-1: Carnitine Palmitoyl Transferase 1; DAG: Diacylglycerol; FAS: Fatty Acyl-CoA Synthase; FoxO1: Forkhead box protein 01; Fructose-1P: Fructose 1-Phosphate; GLUT2: Glucose Transporter 2; IR: Insulin Receptor; IRS-1: Insulin Receptor Substrate 1; JNK-1: C-Jun-<span class="html-italic">N</span> terminal kinase-1; NAFLD: Non-Alcoholic Fat Liver Disease; PEPCK: Phosphoenolpyruvate Carboxykinase; PGC-1α: Peroxisome Proliferator-Activated Receptor-Gama Coactivator 1 Alpha; PGC-1β: Peroxisome Proliferator-Activated Receptor-Gama Coactivator 1 Beta; PKC: Protein Kinase C; ROS: Reactive Oxygen Species; SIRT-1: Sirtuin-1; SREBP1c: Sterol Regulatory Element-Binding Protein 1c; TG: Triglycerides; VLDL: Very Low Density Lipoprotein.</p>
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<p>Exercise prevents and treats the deleterious effects of high consumption of fructose. In addition to promoting an increase in energy expenditure, physical exercise consistently attenuates inflammation and oxidative stress related to excessive consumption of fructose, as reflected in positive changes both in lipid profile and fat metabolism. In this way, insulin resistance and hyperinsulinaemia are diminished, collaborating with the prevention and treatment of diseases such as hepatic steatosis and type 2 diabetes. HDL: High-Density Lipoprotein; LDL: Low-Density Lipoprotein.</p>
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Article
The Sodium Content of Processed Foods in South Africa during the Introduction of Mandatory Sodium Limits
by Sanne A. E. Peters, Elizabeth Dunford, Lisa J. Ware, Teresa Harris, Adele Walker, Mariaan Wicks, Tertia Van Zyl, Bianca Swanepoel, Karen E. Charlton, Mark Woodward, Jacqui Webster and Bruce Neal
Nutrients 2017, 9(4), 404; https://doi.org/10.3390/nu9040404 - 20 Apr 2017
Cited by 51 | Viewed by 9982
Abstract
Background: In June 2016, the Republic of South Africa introduced legislation for mandatory limits for the upper sodium content permitted in a wide range of processed foods. We assessed the sodium levels of packaged foods in South Africa during the one-year period leading [...] Read more.
Background: In June 2016, the Republic of South Africa introduced legislation for mandatory limits for the upper sodium content permitted in a wide range of processed foods. We assessed the sodium levels of packaged foods in South Africa during the one-year period leading up to the mandatory implementation date of the legislation. Methods: Data on the nutritional composition of packaged foods was obtained from nutrition information panels on food labels through both in-store surveys and crowdsourcing by users of the HealthyFood Switch mobile phone app between June 2015 and August 2016. Summary sodium levels were calculated for 15 food categories, including the 13 categories covered by the sodium legislation. The percentage of foods that met the government’s 2016 sodium limits was also calculated. Results: 11,065 processed food items were included in the analyses; 1851 of these were subject to the sodium legislation. Overall, 67% of targeted foods had a sodium level at or below the legislated limit. Categories with the lowest percentage of foods that met legislated limits were bread (27%), potato crisps (41%), salt and vinegar flavoured snacks (42%), and raw processed sausages (45%). About half (49%) of targeted foods not meeting the legislated limits were less than 25% above the maximum sodium level. Conclusion: Sodium levels in two-thirds of foods covered by the South African sodium legislation were at or below the permitted upper levels at the mandatory implementation date of the legislation and many more were close to the limit. The South African food industry has an excellent opportunity to rapidly meet the legislated requirements. Full article
(This article belongs to the Special Issue Reducing Dietary Sodium and Improving Human Health)
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<p>Foods targeted by the sodium legislation according to 2016 sodium limits. Region shaded in green is for foods with sodium levels at or below the sodium limit. The regions shaded in yellow, orange, red, and dark red are for foods with sodium levels 0%–25%, 25%–50%, 50%–100%, or more than 100% above the sodium limit. The maximum total sodium levels allowed in food categories covered by the sodium legislation are given in <a href="#nutrients-09-00404-t001" class="html-table">Table 1</a>. Current sodium levels for targeted foods are provided in <a href="#nutrients-09-00404-t002" class="html-table">Table 2</a>.</p>
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<p>Mean sodium levels of processed meat subcategories in mg per 100 g. Green bars represent meat categories not targeted by the sodium legislation. Red bars represent meat categories targeted by the sodium legislation.</p>
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Article
Genistein Ameliorates Ischemia/Reperfusion-Induced Renal Injury in a SIRT1-Dependent Manner
by Wei-Fang Li, Kang Yang, Ping Zhu, Hong-Qian Zhao, Yin-Hong Song, Kuan-Can Liu and Wei-Feng Huang
Nutrients 2017, 9(4), 403; https://doi.org/10.3390/nu9040403 - 20 Apr 2017
Cited by 40 | Viewed by 7072
Abstract
Renal ischemia/reperfusion (I/R) injury continues to be a complicated situation in clinical practice. Genistein, the main isoflavone found in soy products, is known to possess a wide spectrum of biochemical and pharmacological activities. However, the protective effect of genistein on renal I/R injury [...] Read more.
Renal ischemia/reperfusion (I/R) injury continues to be a complicated situation in clinical practice. Genistein, the main isoflavone found in soy products, is known to possess a wide spectrum of biochemical and pharmacological activities. However, the protective effect of genistein on renal I/R injury has not been well investigated. In the current study, we explore whether genistein exhibits its renal-protective effects through SIRT1 (Sirtuin 1) in I/R-induced mice model. We found the treatment of genistein significantly reduced renal I/R-induced cell death, simultaneously stimulating renal cell proliferation. Meanwhile, SIRT1 expression was up-regulated following the administration of genistein in renal region. Furthermore, pharmacological inhibition or shRNA-mediated depletion of SIRT1 significantly reversed the protective effect of genistein on renal dysfunction, cellular damage, apoptosis, and proliferation following I/R injury, suggesting an indispensible role of the increased SIRT1 expression and activity in this process. Meanwhile, the reduced p53 and p21 expression and increased PCNA (Proliferating Cell Nuclear Antigen) expression were blocked after the depletion of SIRT1 compared with the genistein treatment group in the renal I/R process. Hence, our results provided further experimental basis for the potential use of genistein for the treatment of kidney disease with deficiency of SIRT1 activity. Full article
(This article belongs to the Special Issue Effects of Polyphenol-Rich Foods on Human Health)
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<p>Effect of genistein on kidney injury following I/R injury. In the sham group, mice received the same volume of vehicle without I/R; in the I/R group, mice received the same volume of vehicle with I/R; in the G5 group, mice were pre-treated with 5 mg/kg genistein following I/R; in the G10 group, mice were pre-treated with 10 mg/kg genistein following I/R; and in the G15 group, mice were treated with 15 mg/kg genistein following I/R. The mice were decapitated after 24 h of reperfusion for further analysis. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>a</b>) The Scr levels and BUN levels were examined 24 h after surgery; (<b>b</b>) A semi-quantitative assessment of the lesion was performed by a pathologist in a blinded manner according to the ATN–scoring system. Each tubular segment visible in the cortex and the outer medulla was evaluated; (<b>c</b>) Representative images of the cortex and outer medulla in different groups stained with H&amp;E. Original magnification, 400×. The black arrows indicate the areas of I/R-induced tissue damages.</p>
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<p>Effect of genistein on SIRT1 expression following I/R injury. Mice were treated as described in <a href="#nutrients-09-00403-f001" class="html-fig">Figure 1</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>a</b>) Western blots analysis for SIRT1 expression in mouse kidney tissues. Densitometric analysis of the SIRT1 expression by Image-Pro Plus 6.0. GAPDH was calibrated; (<b>b</b>) Representative images of SIRT1 expression in the kidney, as determined by IHC. Original magnification, 400×. The black arrows indicate the positive cells.</p>
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<p>Effect of genistein on the cellular apoptosis and proliferation following I/R injury. Mice were treated as described in <a href="#nutrients-09-00403-f001" class="html-fig">Figure 1</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>a</b>) Representative photomicrograph of TUNEL-positive cells stained kidney tissues from the I/R and G15 groups and the percentage of positive cells is illustrated; (<b>b</b>) Cleaved caspase-3 and pro-caspase-3 expression was analyzed by western blotting; (<b>c</b>) Representative photomicrograph of PCNA-positive cells stained kidney tissues from the I/R and G15 groups and the percentage of positive cells is illustrated. Original magnification, 400×. The black arrows indicate the positive cells.</p>
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<p>Sirtinol abolishes the protective effect of genistein on renal function and histology in I/R-induced injury. In the vehicle group, mice received the same volume of vehicle; in the Sirtinol group, mice were pre-treated with 1 mg/kg Sirtinol; in the G15 group, mice were pre-treated with 15 mg/kg genistein; in the Sirtinol + G15 group, mice were treated with 15 mg/kg genistein and 1 mg/kg Sirtinol. Ischemia was induced in all of the groups. The mice were decapitated at 24 h of the reperfusion period for further analysis. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. The Scr (<b>a</b>, <b>left</b>) levels and BUN (<b>a</b>, <b>right</b>) levels were examined 24 h after reperfusion. (<b>b</b>, <b>left</b>) Representative images of the cortex and outer medulla from the G15 and G15 + Sirtinol groups stained with H&amp;E. Original magnification, 400×. The black arrows indicate the areas of I/R-induced tissue damages. (<b>b</b>, <b>right</b>) A semi-quantitative assessment of the lesion was performed by a pathologist in a blinded manner according to the ATN–scoring system. Each tubular segment visible in the cortex and outer medulla was evaluated.</p>
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<p>Mice were treated as described in <a href="#nutrients-09-00403-f004" class="html-fig">Figure 4</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Vehicle; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. G15. (<b>a</b>) Representative photomicrograph of TUNEL-positive from the G15 and G15 + Sirtinol groups and the percentage of positive cells were illustrated; (<b>b</b>) Representative photomicrograph of PCNA-positive from the G15 and G15 + Sirtinol groups and the percentage of positive cells were illustrated. Original magnification, 400×. The black arrows indicate the positive cells.</p>
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<p>SIRT1 depletion abrogates the protective effect of genistein on renal function and histology in I/R-induced injury. In the LV-control, mice were injected with lentivirus carrying scrambled shRNA and pre-treated with the same volume of vehicle; in the LV-shSIRT1 group, mice were injected with lentivirus carrying SIRT1 shRNA; in the G15 group, mice were injected with lentivirus carrying scrambled shRNA and were pre-treated with 15 mg/kg genistein; in the LV-shSIRT1 + G15 group, mice were injected with lentivirus carrying SIRT1 shRNA and were pre-treated with 15 mg/kg genistein. Ischemia was induced in all of the groups. The mice were decapitated after 24 h of reperfusion for further analysis. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. The Scr (<b>a</b>, <b>left</b>) levels and BUN (<b>a</b>, <b>right</b>) levels were examined 24 h after reperfusion. (<b>b</b>, <b>left</b>) Representative images of the cortex and outer medulla from G15 and G15 + LV-shSIRT1 groups stained with H&amp;E. Original magnification, 400×. The black arrows indicate the areas of I/R-induced tissue damages. (<b>b</b>, <b>right</b>) Semi-quantitative assessment of the lesion was performed by a pathologist in a blinded manner according to the ATN-scoring system. Each tubular segment visible in the cortex and outer medulla was evaluated.</p>
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<p>Effect of SIRT1 depletion on protein expression following I/R-induced renal injury. Mice were treated as described in <a href="#nutrients-09-00403-f006" class="html-fig">Figure 6</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. LV-control; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. G15. (<b>a</b>) Representative western blots for p53, Acetyl-p53, p21, and PCNA expression in mouse kidney tissues; (<b>b</b>) Densitometric analysis of p53, p21, and PCNA expression by Image-Pro Plus 6.0. GAPDH was calibrated; (<b>c</b>) Densitometric analysis of Acetyl-p53 expression by Image-Pro Plus 6.0. Total p53 was calibrated.</p>
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<p>Proposed scheme for the roles of SIRT1, p53, and other molecules in the protective effect of genistein on I/R-induced renal injury. Genistein treatment significantly reduced renal I/R-induced cell death, simultaneously stimulating renal cell proliferation. Paralleling the protective effect of genistein against I/R-induced renal injury, SIRT1 expression was upregulated upon the administration of genistein. Genistein reduced p53, p21, and cleaved caspase-3 expression and increased PCNA expression. Pharmacological inhibition or shRNA-mediated depletion of SIRT1 significantly reversed the effect of genistein on renal dysfunction, cellular damage, apoptosis, and proliferation following I/R injury. The reduced p53, p21 expression, and increased PCNA expression were blunted after the depletion of SIRT1 compared with the genistein treatment group in the renal I/R process.</p>
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<p>Effect of genistein on renal function at different time points. In the sham group, mice received the same volume of vehicle without I/R; in the I/R group, mice received the same volume of vehicle with I/R; in the G15 group, mice were treated with 15 mg/kg genistein. The mice were decapitated after 12, 24, 48, and 72 h of reperfusion for renal functional analysis. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. The Scr (<b>A</b>) levels and BUN (<b>B</b>) levels were examined 12, 24, 48, and 72 h after reperfusion.</p>
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<p>Effect of genistein on renal histology in I/R-induced injury at different time points. Mice were treated as described in supplemental <a href="#nutrients-09-00403-f009" class="html-fig">Figure A1</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>Top</b>) Representative images of the cortex and outer medulla at 12, 24, 48, and 72 h of the reperfusion period stained with H&amp;E. Original magnification, 400×; (<b>Bottom</b>) Semi-quantitative assessment of the lesion was performed by a pathologist in a blinded manner according to the ATN–scoring system. Each tubular segment visible in the cortex and outer medulla was evaluated.</p>
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<p>Effect of genistein on SIRT1 mRNA expression following I/R injury. In the sham group, mice received the same volume of vehicle without I/R; in the I/R group, mice received the same volume of vehicle with I/R; in the G5 group, mice were pre-treated with 5 mg/kg genistein following I/R; in the G10 group, mice were pre-treated with 10 mg/kg genistein following I/R; in the G15 group, mice were treated with 15 mg/kg genistein. The mice were decapitated at 24 h of the reperfusion period for further analysis. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. The SIRT1 mRNA levels for specific genes were normalized to 18S rRNA levels.</p>
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<p>Sirtinol reverses the effect of genistein on apoptosis in I/R-induced acute renal injury. Mice were treated as described in supplemental <a href="#nutrients-09-00403-f004" class="html-fig">Figure 4</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Vehicle; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. G15. (<b>A</b>) Representative photomicrograph of cleaved caspase-3-stained kidney tissues from the G15 and G15 + Sirtinol groups. Original magnification, 400×; (<b>B</b>) Cleaved caspase-3-positive cells were counted, and the percentage of positive cells is illustrated. The black arrows indicate positive cells.</p>
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<p>Sirtinol abrogates the effect of genistein on PCNA expression in I/R-induced acute renal injury. Mice were treated as described in supplemental <a href="#nutrients-09-00403-f004" class="html-fig">Figure 4</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Vehicle; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. G15. (<b>A</b>) Representative western blots for PCNA expression in mice kidney tissues; (<b>B</b>) Densitometric analysis of the PCNA expression by Image-Pro Plus 6.0. GAPDH was calibrated.</p>
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<p>Western blot analyses demonstrating the knock-down of SIRT1 in kidney tissues. Seventy-two hours later after the injection of LV-control or LV-shSIRT1, genistein, or the same volume of vehicle. For the LV-control group and G15 groups, mice were pre-treated with vehicle; for the LV-shSIRT1 group, mice were pre-treated with vehicle; for the G15 and LV-shSIRT1 + G15 groups, mice were pre-treated with 15 mg/kg genistein. Ischemia was induced in all of the groups. The mice were decapitated after 24 h of reperfusion for the western blot analysis. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>A</b>) Representative western blots for SIRT1 expression in mouse kidney tissues; (<b>B</b>) Densitometric analysis of the SIRT1 expression by Image-Pro Plus 6.0. GAPDH was calibrated.</p>
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<p>IHC analyses demonstrating the knock-down of SIRT1 in kidney tissues. Mice were treated as described in supplemental <a href="#nutrients-09-00403-f007" class="html-fig">Figure 7</a>. Representative photomicrograph of SIRT1-stained kidney tissues from the G15 and G15 + LV-shSIRT1 groups. Original magnification, 400×. The black arrows indicate positive cells.</p>
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<p>SIRT1 depletion reverses the effect of genistein on apoptosis in I/R-induced acute renal injury. Mice were treated as described in supplemental <a href="#nutrients-09-00403-f007" class="html-fig">Figure 7</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>A</b>) Representative photomicrograph of TUNEL-stained kidney tissues from the G15 and G15 + Sirtinol groups. Original magnification, 400×; (<b>B</b>) TUNEL-positive cells were counted and the percentage of positive cells is illustrated. The black arrows indicate positive cells.</p>
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<p>SIRT1 depletion reverses the increased effect of genistein on cellular proliferation in I/R-induced acute renal injury. Mice were treated as described in supplemental <a href="#nutrients-09-00403-f007" class="html-fig">Figure 7</a>. The data were expressed as the mean ± SEM; <span class="html-italic">n</span> = 6; * <span class="html-italic">p</span> &lt; 0.05 vs. Sham; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. I/R. (<b>A</b>) Representative photomicrograph of PCNA-stained kidney tissues from the G15 and G15 + Sirtinol groups. Original magnification, 400×; (<b>B</b>) PCNA-positive cells were counted, and the percentage of positive cells is illustrated. The black arrows indicate positive cells.</p>
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Article
Chocolate Consumption and Risk of Heart Failure: A Meta-Analysis of Prospective Studies
by Fei Gong, Shuyuan Yao, Jing Wan and Xuedong Gan
Nutrients 2017, 9(4), 402; https://doi.org/10.3390/nu9040402 - 20 Apr 2017
Cited by 25 | Viewed by 9216
Abstract
Epidemiological studies have shown inconsistent findings on the association between chocolate consumption and risk of heart failure (HF). We, therefore, performed a meta-analysis of prospective studies to determine the role of chocolate intake in the prevention of HF. We searched databases of PubMed, [...] Read more.
Epidemiological studies have shown inconsistent findings on the association between chocolate consumption and risk of heart failure (HF). We, therefore, performed a meta-analysis of prospective studies to determine the role of chocolate intake in the prevention of HF. We searched databases of PubMed, Web of Science, and Scopus through December 2016 and scrutinized the reference lists of relevant literatures to identify eligible studies. Study-specific hazard ratios (HRs) and 95% confidence intervals (CIs) were aggregated using random effect models. The dose–response relationship between chocolate consumption and incident HF was also assessed. This meta-analysis is registered with PROSPERO, number CRD42017054230. Five prospective studies with 106,109 participants were finally included. Compared to no consumption of chocolate, the pooled HRs (95% CIs) of HF were 0.86 (0.82–0.91) for low-to-moderate consumption (<7 servings/week) and 0.94 (0.80–1.09) for high consumption (≥7 servings/week). In dose–response meta-analysis, we detected a curve linear relationship between chocolate consumption and risk of HF (p for nonlinearity = 0.005). Compared with non-consumption, the HRs (95% CIs) of HF across chocolate consumption levels were 0.92 (0.88–0.97), 0.86 (0.78–0.94), 0.93 (0.85–1.03), and 1.07 (0.92–1.23) for 1, 3, 7, and 10 servings/week, respectively. In conclusion, chocolate consumption in moderation may be associated with a decreased risk of HF. Full article
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<p>Flow diagram of study selection.</p>
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<p>Hazard ratios of heart failure for low-to-moderate and high chocolate consumption.</p>
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<p>Hazard ratios of heart failure for low and moderate chocolate consumption.</p>
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<p>Dose–response relationship between chocolate consumption and risk of heart failure.</p>
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Review
Dried Plums, Prunes and Bone Health: A Comprehensive Review
by Taylor C. Wallace
Nutrients 2017, 9(4), 401; https://doi.org/10.3390/nu9040401 - 19 Apr 2017
Cited by 50 | Viewed by 24394
Abstract
The 2015–2020 Dietary Guidelines for Americans advocate for increasing fruit intake and replacing energy-dense foods with those that are nutrient-dense. Nutrition across the lifespan is pivotal for the healthy development and maintenance of bone. The National Osteoporosis Foundation estimates that over half of [...] Read more.
The 2015–2020 Dietary Guidelines for Americans advocate for increasing fruit intake and replacing energy-dense foods with those that are nutrient-dense. Nutrition across the lifespan is pivotal for the healthy development and maintenance of bone. The National Osteoporosis Foundation estimates that over half of Americans age 50+ have either osteoporosis or low bone mass. Dried plums, also commonly referred to as prunes, have a unique nutrient and dietary bioactive profile and are suggested to exert beneficial effects on bone. To further elucidate and summarize the potential mechanisms and effects of dried plums on bone health, a comprehensive review of the scientific literature was conducted. The PubMed database was searched through 24 January 2017 for all cell, animal, population and clinical studies that examined the effects of dried plums and/or extracts of the former on markers of bone health. Twenty-four studies were included in the review and summarized in table form. The beneficial effects of dried plums on bone health may be in part due to the variety of phenolics present in the fruit. Animal and cell studies suggest that dried plums and/or their extracts enhance bone formation and inhibit bone resorption through their actions on cell signaling pathways that influence osteoblast and osteoclast differentiation. These studies are consistent with clinical studies that show that dried plums may exert beneficial effects on bone mineral density (BMD). Long-term prospective cohort studies using fractures and BMD as primary endpoints are needed to confirm the effects of smaller clinical, animal and mechanistic studies. Clinical and prospective cohort studies in men are also needed, since they represent roughly 29% of fractures, and likewise, diverse race and ethnic groups. No adverse effects were noted among any of the studies included in this comprehensive review. While the data are not completely consistent, this review suggests that postmenopausal women may safely consume dried plums as part of their fruit intake recommendations given their potential to have protective effects on bone loss. Full article
(This article belongs to the Special Issue Dietary Bioactives and Bone Health)
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Article
Mismatch between Probiotic Benefits in Trials versus Food Products
by Mary J. Scourboutakos, Beatriz Franco-Arellano, Sarah A. Murphy, Sheida Norsen, Elena M. Comelli and Mary R. L’Abbé
Nutrients 2017, 9(4), 400; https://doi.org/10.3390/nu9040400 - 19 Apr 2017
Cited by 24 | Viewed by 29677 | Correction
Abstract
Probiotic food products contain a variety of different bacterial strains and may offer different health effects. The objective was to document the prevalence and dosage of probiotic strains in the Canadian food supply and to review the literature investigating these strains in order [...] Read more.
Probiotic food products contain a variety of different bacterial strains and may offer different health effects. The objective was to document the prevalence and dosage of probiotic strains in the Canadian food supply and to review the literature investigating these strains in order to understand what health benefits these products may offer. The Food Label Information Program was used to identify probiotic-containing products in the food supply. PubMed, Web of Science, and Embase were searched for randomized controlled trials that tested the health effects of these strains in humans. There were six probiotic strains/strain combinations identified in the food supply. Thirty-one studies investigated these strains and found that they are associated with decreased diarrhea and constipation, improved digestive symptoms, glycemic control, antioxidant status, blood lipids, oral health, and infant breastfeeding outcomes, as well as enhanced immunity and support for Helicobacter pylori eradication. There were a limited number of studies investigating these strains. Many studies were funded by the food industry and tested dosages that were up to twenty-five times the dosage found in most food products. Probiotic food products could have health benefits not currently reported on their labels. However, many dosages are too low to provide the benefits demonstrated in clinical trials. Further research is needed to enable more effective use of these functional foods. Full article
(This article belongs to the Special Issue Prebiotics and Probiotics)
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<p>Identification of eligible studies.</p>
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Article
Nutritional Status Predicts 10-Year Mortality in Patients with End-Stage Renal Disease on Hemodialysis
by Shin Sook Kang, Jai Won Chang and Yongsoon Park
Nutrients 2017, 9(4), 399; https://doi.org/10.3390/nu9040399 - 18 Apr 2017
Cited by 77 | Viewed by 8801
Abstract
Protein-energy wasting (PEW) is associated with mortality in patients with end-stage renal disease (ESRD) on maintenance hemodialysis. The correct diagnosis of PEW is extremely important in order to predict clinical outcomes. However, it is unclear which parameters should be used to diagnose PEW. [...] Read more.
Protein-energy wasting (PEW) is associated with mortality in patients with end-stage renal disease (ESRD) on maintenance hemodialysis. The correct diagnosis of PEW is extremely important in order to predict clinical outcomes. However, it is unclear which parameters should be used to diagnose PEW. Therefore, this retrospective observational study investigated the relationship between mortality and nutritional parameters in ESRD patients on maintenance hemodialysis. A total of 144 patients were enrolled. Nutritional parameters, including body mass index, serum albumin, dietary intake, normalized protein catabolic rate (nPCR), and malnutrition inflammation score (MIS), were measured at baseline. Fifty-three patients died during the study. Survivors had significantly higher nPCR (1.10 ± 0.24 g/kg/day vs. 1.01 ± 0.21 g/kg/day; p = 0.048), energy intake (26.7 ± 5.8 kcal/kg vs. 24.3 ± 4.2 kcal/kg; p = 0.009) and protein intake (0.91 ± 0.21 g/kg vs. 0.82 ± 0.24 g/kg; p = 0.020), and lower MIS (5.2 ± 2.3 vs. 6.1 ± 2.1, p = 0.039). In multivariable analysis, energy intake <25 kcal/kg (HR 1.860, 95% CI 1.018–3.399; p = 0.044) and MIS > 5 (HR 2.146, 95% CI 1.173–3.928; p = 0.013) were independent variables associated with all-cause mortality. These results suggest that higher MIS and lower energy intake are harmful to ESRD patients on maintenance hemodialysis. Optimal energy intake could reduce mortality in these patients. Full article
(This article belongs to the Special Issue Nutrition and Chronic Kidney Disease)
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<p>Kaplan–Meier survival curves showing 120-month survival according to nutritional markers: (<b>a</b>) Malnutrition Inflammation Score; (<b>b</b>) energy intake; (<b>c</b>) protein intake; and (<b>d</b>) nPCR.</p>
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<p>Kaplan–Meier survival curves showing 120-month survival according to nutritional markers: (<b>a</b>) Malnutrition Inflammation Score; (<b>b</b>) energy intake; (<b>c</b>) protein intake; and (<b>d</b>) nPCR.</p>
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Comment
Comments to Article by Solah VA et al., Nutrients 2017, 9, 149
by Vladimir Vuksan, Elena Jovanovski, Andreea Zurbau and Allison Komishon
Nutrients 2017, 9(4), 398; https://doi.org/10.3390/nu9040398 - 18 Apr 2017
Viewed by 3675
Abstract
Dear Editor, We read with interest the article published in the 16 February 2017 issue of The Journal, titled “Effect of Fibre Supplementation on Body Weight and Composition, Frequency of Eating and Dietary Choice in Overweight Individuals” by Solah VA et al. [1].[...] [...] Read more.
Dear Editor, We read with interest the article published in the 16 February 2017 issue of The Journal, titled “Effect of Fibre Supplementation on Body Weight and Composition, Frequency of Eating and Dietary Choice in Overweight Individuals” by Solah VA et al. [1].[...] Full article
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Article
Do Chinese Children Get Enough Micronutrients?
by Huijun Wang, Dantong Wang, Yifei Ouyang, Feifei Huang, Gangqiang Ding and Bing Zhang
Nutrients 2017, 9(4), 397; https://doi.org/10.3390/nu9040397 - 18 Apr 2017
Cited by 50 | Viewed by 8368
Abstract
The aim of this study was to examine usual daily micronutrient intake of Chinese children based on data from the 2011 China Health and Nutrition Survey. We analyzed data from 4 to 17-year-old participants, who provided dietary data on three consecutive days combined [...] Read more.
The aim of this study was to examine usual daily micronutrient intake of Chinese children based on data from the 2011 China Health and Nutrition Survey. We analyzed data from 4 to 17-year-old participants, who provided dietary data on three consecutive days combined with the household weighing method in 2011. Usual daily intake of each nutrient was estimated using a mixed effects model based on the China Food Composition published in 2009. The means, medians and percentages below Estimated Average Requirements (EAR) were reported for selected micronutrients, including calcium, sodium, potassium, iron, zinc, selenium, vitamin A, thiamine, riboflavin and vitamin C. For sodium and potassium, the means and the distribution of intakes were compared to the Adequate Intake (AI) level. The average usual daily intakes of all micronutrients increase with age, and the intakes of boys were found to be higher than girls in the same age group. The average calcium intake increased from 272 mg/day in 4–6 years to 391 mg/day in 14–17 years, but the percentage of inadequate calcium intake remained very high (>96%). The prevalence of inadequacy of calcium was the highest among the mineral nutrients reported in this study. As the requirements of micronutrients increased with age, the percentage of subjects with inadequate intake increased in the 11–17 years age groups. Among 14–17 years group, the percentages of study participants with dietary intakes of calcium, iron, zinc, selenium, vitamin A, thiamine, riboflavin and vitamin C below the EAR were 96.8%, 18.8%, 37.6%, 72.8%, 36.8%, 91.8%. 85.9% and 75.5%, respectively. Among 11–13 years group, the percentages of study participants with dietary intakes of iron, zinc and vitamin A below the EAR were 23.5%, 41.5%, and 41.6%, respectively. Thus, micronutrient deficiency is a problem in Chinese children. Nutrition education and intervention programs are needed to address these nutritional gaps. Full article
(This article belongs to the Special Issue Chinese National Nutrition Survey 2012)
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Article
Cereal Consumption among Subjects with Celiac Disease: A Snapshot for Nutritional Considerations
by Francesco Valitutti, Donatella Iorfida, Caterina Anania, Chiara Maria Trovato, Monica Montuori, Salvatore Cucchiara and Carlo Catassi
Nutrients 2017, 9(4), 396; https://doi.org/10.3390/nu9040396 - 18 Apr 2017
Cited by 27 | Viewed by 6600
Abstract
Background: To our knowledge no study has focused on the pattern of cereal-based products (CBP) consumption among people with celiac disease (CD). Our study aimed at evaluating the dietary intake of CBP among patients with CD and comparing it with a control population. [...] Read more.
Background: To our knowledge no study has focused on the pattern of cereal-based products (CBP) consumption among people with celiac disease (CD). Our study aimed at evaluating the dietary intake of CBP among patients with CD and comparing it with a control population. Methods: Eighty-two volunteers with CD and 77 non-CD volunteers enrolled throughout Italy were asked to register their consumption of CBP on specific diaries for three days. Results: CD patients’ median three-day intake of biscuits and crackers was higher compared to controls (65.8 g vs. 22.7 g and 44.7 g vs. 10.6 g, p < 0.05 respectively, Mann–Whitney test). A significant difference was observed also comparing the two groups for median three-day bread consumption, with the CD group consuming less bread than controls (109.5 g vs. 150.7 g, p < 0.05, Mann–Whitney test). When assessing regional and gender-related CBP consumption patterns, significantly higher rice consumption was found among CD women from Northern Italy compared to CD women from Central and Southern Italy (p = 0.006 and p = 0.002 respectively, Fisher’s exact test). No other significant differences were observed. Conclusions: Our results provide a snapshot of the overall consumption of CBP among Italian subjects with CD. Altogether, these data show that, despite minor differences, dietary consumption of CBP among CD patients is similar to the general population. Full article
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<p>Median three-day consumption of cereal-based products in 82 celiac patients and 77 healthy controls. Data are expressed in grams.</p>
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<p>Daily cereal-based product consumption pattern in CD patients and controls according to food processing: raw cereals (rice, polenta, other cereals) vs. processed cereal-based products (sweet pastries, bread, pasta, homemade cakes, biscuits, crackers, breakfast cereals, and breadcrumbs).</p>
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<p>Raw cereal consumption of CD patients.</p>
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<p>Raw cereal consumption of the control group.</p>
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Review
Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review
by Cristiana Caliceti, Donato Calabria, Aldo Roda and Arrigo F. G. Cicero
Nutrients 2017, 9(4), 395; https://doi.org/10.3390/nu9040395 - 18 Apr 2017
Cited by 172 | Viewed by 27153
Abstract
There is a direct relationship between fructose intake and serum levels of uric acid (UA), which is the final product of purine metabolism. Recent preclinical and clinical evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, and cardiovascular [...] Read more.
There is a direct relationship between fructose intake and serum levels of uric acid (UA), which is the final product of purine metabolism. Recent preclinical and clinical evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, and cardiovascular disease. It is probably also an independent risk factor for chronic kidney disease, Type 2 diabetes, and cognitive decline. These relationships have been observed for high serum UA levels (>5.5 mg/dL in women and >6 mg/dL in men), but also for normal to high serum UA levels (5–6 mg/dL). In this regard, blood UA levels are much higher in industrialized countries than in the rest of the world. Xanthine-oxidase inhibitors can reduce UA and seem to minimize its negative effects on vascular health. Other dietary and pathophysiological factors are also related to UA production. However, the role of fructose-derived UA in the pathogenesis of cardiometabolic disorders has not yet been fully clarified. Here, we critically review recent research on the biochemistry of UA production, the relationship between fructose intake and UA production, and how this relationship is linked to cardiometabolic disorders. Full article
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<p>Uric acid formation through xanthine oxidase activity. (<b>A</b>) Under ischemic or inflammatory conditions, xanthine dehydrogenase (XDH) is converted to xanthine oxidase (XO) via the oxidation of sulfhydryl residues or proteolysis of XDH. In the presence of oxygen, XO catalyses the oxidation of hypoxanthine to xanthine and then to uric acid (UA), with consequent production of the superoxide anion (O<sub>2</sub><sup>−</sup>) and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). The competitive antagonist allopurinol is converted in the active form, oxypurinol, via XO activity, acting as an XO inhibitor; (<b>B</b>) During hypoxanthine conversion to xanthine and then UA, high levels of H<sub>2</sub>O<sub>2</sub> and O<sub>2</sub><sup>−</sup> are produced and converted to O<sub>2</sub> and H<sub>2</sub>O<sub>2</sub>, spontaneously or in a reaction catalyzed by the enzyme superoxide dismutase (SOD).</p>
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<p>Fructose-induced uric acid formation: risk factor biomarkers. In hepatocytes, fructokinase catalyzes the rapid phosphorylation of fructose to fructose-1-phosphate, using ATP as a phosphate donor. Intracellular phosphate (Pi) levels decrease, stimulating the activity of AMP deaminase (AMPD). AMPD converts AMP to inosine monophosphate (IMP). IMP is metabolized to inosine, which is further degraded to xanthine and hypoxanthine by xanthine oxidase (XO), ultimately generating uric acid (UA). UA can react with nitric oxide (NO), reducing NO bioavailability and inducing dinucleotide phosphate oxidase (NOX) activation and mitochondrial dysfunction. In turn, this promotes oxidative stress and endothelial dysfunction. Fructose per se can also induce oxidative stress.</p>
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Article
Serum Insulin-Like Growth Factor Axis and the Risk of Pancreatic Cancer: Systematic Review and Meta-Analysis
by Yuanfeng Gong, Bingyi Zhang, Yadi Liao, Yunqiang Tang, Cong Mai, Tiejun Chen and Hui Tang
Nutrients 2017, 9(4), 394; https://doi.org/10.3390/nu9040394 - 18 Apr 2017
Cited by 17 | Viewed by 5572
Abstract
Objective: To investigate the association between serum concentration of insulin-like growth factor (IGF) and the risk of pancreatic cancer (PaC). Methods: We identified eligible studies in Medline and EMBASE databases (no reference trials from 2014 to 2016) in addition to the reference lists [...] Read more.
Objective: To investigate the association between serum concentration of insulin-like growth factor (IGF) and the risk of pancreatic cancer (PaC). Methods: We identified eligible studies in Medline and EMBASE databases (no reference trials from 2014 to 2016) in addition to the reference lists of original studies and review articles on this topic. A summary of relative risks with 95% confidence intervals (CI) was calculated using a random-effects model. The heterogeneity between studies was assessed using Cochran Q and I2 statistics. Results: Ten studies (seven nested case-control studies and three retrospective case-control studies) were selected as they met our inclusion criteria in this meta-analysis. All these studies were published between 1997 and 2013. The current data suggested that serum concentrations of IGF-I, IGF-II and insulin-like growth factor binding protein-3 (IGFBP-3)in addition to the IGF-I/IGFBP-3 ratio were not associated with an increased risk of PaC (Summary relative risks (SRRs) = 0.92, 95% CI: 0.67–1.16 for IGF-I; SRRs = 0.84, 95% CI: 0.54–1.15 for IGF-II; SRRs = 0.93, 95% CI: 0.69–1.17 for IGFBP-3; SRRs = 0.97, 95% CI: 0.71–1.23 for IGF-I/IGFBP-3 ratio). There was no publication bias in the present meta-analysis. Conclusion: Serum concentrations of IGF-I, IGF-II, IGFBP-1 and IGFBP-3 as well as the IGF-I/IGFBP-3 ratio were not associated with increased risk of PaC. Full article
(This article belongs to the Special Issue Nutrients, Infectious and Inflammatory Diseases)
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<p>Flow chart of selection of studies included in the meta-analysis.</p>
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<p>Forest plot of insulin-like growth factor (IGF)-I and pancreatic cancer (PaC) risk for: (<b>a</b>) nested case-control studies and (<b>b</b>) case-control studies.</p>
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<p>Forest plot of insulin-like growth factor (IGF-II) and pancreatic cancer (PaC) risk. CI = Confidence interval; ES = Effect size.</p>
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<p>Forest plot of Insulin-like growth factor binding protein (IGFBP)-3 and pancreatic cancer (PaC) risk. CI = Confidence interval; ES = Effect size.</p>
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<p>Forest plot of the insulin-like growth factor (IGF)-I/Insulin-like growth factor binding protein (IGFBP)-3 ratio and pancreatic cancer (PaC) risk. CI = Confidence interval; ES = Effect size.</p>
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<p>Funnel plot of studies evaluating the association of (<b>a</b>) insulin-like growth factor (IGF)-I with pancreatic cancer (PaC) risk (Begg’s test (<span class="html-italic">p</span> = 1.00) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>], Egger’s test (<span class="html-italic">p</span> = 0.794) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>]); and (<b>b</b>) IGFBP-3 with PaC risk (Begg’s test (<span class="html-italic">p</span> = 0.707) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>], Egger’s test (<span class="html-italic">p</span> = 0.785) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>]. RR = Relative risk.</p>
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<p>Funnel plot of studies evaluating the association of (<b>a</b>) insulin-like growth factor (IGF)-I with pancreatic cancer (PaC) risk (Begg’s test (<span class="html-italic">p</span> = 1.00) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>], Egger’s test (<span class="html-italic">p</span> = 0.794) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>]); and (<b>b</b>) IGFBP-3 with PaC risk (Begg’s test (<span class="html-italic">p</span> = 0.707) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>], Egger’s test (<span class="html-italic">p</span> = 0.785) [<a href="#B21-nutrients-09-00394" class="html-bibr">21</a>,<a href="#B22-nutrients-09-00394" class="html-bibr">22</a>,<a href="#B30-nutrients-09-00394" class="html-bibr">30</a>,<a href="#B31-nutrients-09-00394" class="html-bibr">31</a>,<a href="#B32-nutrients-09-00394" class="html-bibr">32</a>,<a href="#B33-nutrients-09-00394" class="html-bibr">33</a>]. RR = Relative risk.</p>
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Article
Differential Effect of Sucrose and Fructose in Combination with a High Fat Diet on Intestinal Microbiota and Kidney Oxidative Stress
by Adriana Rosas-Villegas, Mónica Sánchez-Tapia, Azalia Avila-Nava, Victoria Ramírez, Armando R. Tovar and Nimbe Torres
Nutrients 2017, 9(4), 393; https://doi.org/10.3390/nu9040393 - 16 Apr 2017
Cited by 67 | Viewed by 10644
Abstract
There is controversial information about the adverse effect of sucrose (S) or fructose (F) in the development of obesity. Thus, the purpose of the study was to evaluate the effect of S or F in a high fat diet (HF) on gut microbiota [...] Read more.
There is controversial information about the adverse effect of sucrose (S) or fructose (F) in the development of obesity. Thus, the purpose of the study was to evaluate the effect of S or F in a high fat diet (HF) on gut microbiota and renal oxidative stress. Rats were fed for four months with either high-fat + sucrose (HFS) or high-fat + fructose (HFF) or a control diet (C). Half of the HFS or HFF groups were maintained with the same diet and the other half were switched to the consumption of C. HFS and HFF groups increased 51% and 19% body weight, respectively, compared with the C group. Body fat mass, metabolic inflexibility, glucose intolerance, lipopolysaccharide (LPS), insulin, renal reactive oxygen species (ROS), malondialdehyde (MDA), Nadphox, and Srebp-1 were significantly higher and antioxidant enzymes and lean body mass were significantly lower in the HFS group with respect to the HF-F group. Change in the consumption of HFS or HFF to a C diet ameliorated the insulin and glucose intolerance. The type of carbohydrate differentially modified the microbiota composition, however, both groups significantly decreased C. eutactus with respect to the C group. Thus, metabolic alterations with the HFS diet had a more detrimental effect than HFF. Full article
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Figure 1

Figure 1
<p>Effect of a high fat diet enriched with 5% of sucrose (HFS) or fructose (HFF) in water on body weight (<b>A</b>); fat mass (<b>B</b>); lean mass (<b>C</b>); energy expenditure (<b>D</b>); and oxygen consumption (<b>E</b>). The data are expressed as the mean ± SEM (<span class="html-italic">n</span> = 4). Results were considered statistically significant at <span class="html-italic">p</span> &lt; 0.05. The differences between groups are indicated by letters, where a &gt; b &gt; c. C: control; HFS: high-fat and sucrose; HFS→C high-fat and sucrose, switched to the control diet; HFF: high-fat and fructose; HFS→C: high-fat and fructose, switched to control diet.</p>
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<p>High-fat sucrose (HFS) or high-fat fructose (HFF) diets differentially modified the gut microbiota. Relative abundances of the gut microbiota at the bacterial genus (<b>A</b>); heat map showing the 10 most modified genera (<b>B</b>); relative abundances at the specie level (<b>C</b>); and heat map showing the ten most modified species (<b>D</b>) after the consumption of HFS or HFF diets. Unweighted principal component analysis (PCA) of gut microbiota after the consumption of different diets (<b>E</b>). The closer the spatial distance between samples the more similar they are with respect to both axes (PERMANOVA, <span class="html-italic">p</span> = 0.001). Correlation between serum LPS concentration and percent fat mass (<span class="html-italic">r</span> = 0.95) (<b>F</b>). The data are expressed as the mean ± SEM (<span class="html-italic">n</span> = 4). Results were considered statistically significant at <span class="html-italic">p</span> &lt; 0.05. The differences between groups are indicated by letters, where a &gt; b &gt; c. C: control; HFS: high-fat and sucrose; HFS→C: high-fat and sucrose, switched to the control diet; HFF: high-fat and fructose; HFS→C: high-fat and fructose, switched to control diet.</p>
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<p>Serum biochemical parameters and glucose tolerance test after the consumption of different diets. Serum glucose (<b>A</b>); insulin (<b>B</b>); glucose tolerance test (<b>C</b>); area under the curve after the glucose tolerance test (<b>D</b>); triglycerides (<b>E</b>); total cholesterol (<b>F</b>); LDL cholesterol (<b>G</b>); and lipopolysaccharides (<b>H</b>). The data are expressed as the mean ± SEM (<span class="html-italic">n</span> = 4). Results were considered statistically significant at <span class="html-italic">p</span> &lt; 0.05. The differences between groups are indicated by letters, where a &gt; b &gt; c. C: control; HFS: high-fat and sucrose; HFS→C: high-fat and sucrose, switched to control diet; HFF: high-fat and fructose; HFS→C: high-fat and fructose, switched to control diet.</p>
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<p>Relative protein abundance and oxidative markers in the kidneys of rats fed high-fat sucrose or fructose diets. Protein abundance of toll-like receptor 4 (<b>A</b>); nuclear factor kappa B (<b>B</b>); tumor necrosis factor alpha (<b>C</b>); monocyte chemoattractant protein 1 (<b>D</b>); and uncoupling protein 1 (<b>E</b>). Renal reactive oxygen species (<b>F</b>); malondialdehyde concentration (<b>G</b>); and urinary hydrogen peroxide (<b>H</b>). The data are expressed as the mean ± SEM (<span class="html-italic">n</span> = 4). Results were considered statistically significant at <span class="html-italic">p</span> &lt; 0.05. The differences between groups are indicated by letters, where a &gt; b &gt; c. C: control; HFS: high-fat and sucrose; HFS→C: high-fat and sucrose, switched to the control diet; HFF: high-fat and fructose; HFS→C: high-fat and fructose, switched to the control diet.</p>
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<p>Relative gene expression of inflammatory cytokines, lipogenesis, oxidant, and antioxidant enzymes in kidney. Interleukin 1-β (<b>A</b>); interleukin 6 (<b>B</b>); NADPH oxidase (<b>C</b>); sterol regulatory element-binding protein-1c (<b>D</b>); superoxide dismutase 1 (<b>E</b>); glutathione reductase (<b>F</b>); glutathione peroxidase (<b>G</b>); and catalase (<b>H</b>). The data are expressed as the mean ± SEM (<span class="html-italic">n</span> = 5). Results were considered statistically significant at <span class="html-italic">p</span> &lt; 0.05. The differences between groups are indicated by letters, where a &gt; b &gt; c. C: control; HFS: high-fat and sucrose; HFS→C: high-fat and sucrose, switched to the control diet; HFF: high-fat and fructose; HFS→C: high-fat and fructose, switched to the control diet.</p>
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<p>Graphical summary of differential effects of high fat + sucrose of high fat + fructose on gut microbiota, inflammatory cytokines, insulin resistance, and oxidative stress and lipogenesis in kidney.</p>
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