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        <title>Nutrition &amp; Metabolism - Latest Articles</title>
        <link>http://www.nutritionandmetabolism.com</link>
        <description>The latest research articles published by Nutrition &amp; Metabolism</description>
        <dc:date>2013-05-16T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/39" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/38" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/37" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/36" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/35" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/34" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/33" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/32" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/31" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/10/1/29" />
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/39">
        <title>The effects of pre- and post-exercise consumption of multi-ingredient performance supplements on cardiovascular health and body fat in trained men after six weeks of resistance training: a stratified, randomized, double-blind study</title>
        <description>Background:
The cardiovascular (CV) and metabolic health benefits or risks associated with consumption of multi-ingredient performance supplements (MIPS) in conjunction with periodized resistance training (RT) in resistance-trained men are unknown. This population is a major target audience for performance supplements, and therefore, the purpose of this study was to investigate the combined effect of RT and commercially available pre- and post-exercise performance supplements on CV health and body fat in resistance-trained men.
Methods:
Twenty-four resistance-trained men completed six weeks (three times/week) of periodized RT while either ingesting SHOT 15-min pre-exercise and SYN immediately post-exercise (multi-ingredient performance supplement group: MIPS) or an isocaloric maltodextrin placebo 15-min pre-exercise and immediately post-exercise (Placebo group). Before and after six weeks of RT and supplementation, resting heart rate (HR), blood pressure (BP), total body fat, android fat, gynoid fat, fat-free mass (FFM) and fasting blood measures of glucose, lipids, nitrate/nitrite (NOx), cortisol and high sensitivity C-reactive protein (hs-CRP) were measured. Statistical analysis was conducted using a one-way ANOVA for baseline differences and a 2 x 2 (group x time) repeated measures ANOVA and Tukey post-hoc tests where appropriate. Significance was set at p &lt; 0.05.
Results:
There was no group x time interaction for HR, BP, blood glucose, lipids, NOx, hs-CRP, cortisol concentrations or body fat. However, there was a time effect where significant decreases in body fat (mean +/- SD; MIPS: -1.2 +/- 1.2%; Placebo: -0.9 +/- 1.1%), android fat (MIPS: -1.8 +/- 2.1%; Placebo: -1.6 +/- 2.0%), and gynoid fat (MIPS: -1.3 +/- 1.6%; Placebo: -1.0 +/- 1.4%) for both groups were observed. FFM increased in both groups, and a group x time interaction was observed with MIPS increasing significantly more than the Placebo group (4.2% vs. 1.9%).
Conclusions:
Six weeks of MIPS ingestion and periodized RT does not alter CV health parameters or blood indices of health or body fat more than a Placebo treatment in healthy, resistance-trained men. However, MIPS significantly increased FFM more than Placebo.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/39</link>
                <dc:creator>Michael Ormsbee</dc:creator>
                <dc:creator>Dennison Thomas</dc:creator>
                <dc:creator>William Mandler</dc:creator>
                <dc:creator>Emery Ward</dc:creator>
                <dc:creator>Amber Kinsey</dc:creator>
                <dc:creator>Lynn Panton</dc:creator>
                <dc:creator>Timothy Scheett</dc:creator>
                <dc:creator>Shirin Hooshmand</dc:creator>
                <dc:creator>Emily Simonavice</dc:creator>
                <dc:creator>Jeong-Su Kim</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:39</dc:source>
        <dc:date>2013-05-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-39</dc:identifier>
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        <prism:startingPage>39</prism:startingPage>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/38">
        <title>Effects of low-volume walking programme and vitamin E supplementation on oxidative damage and health-related variables in healthy older adults</title>
        <description>Background:
Both exercise and vitamin E supplementation have been shown to reduce oxidative stress and cardiovascular disease risk in older adults, and when combined there is evidence suggesting that they act synergistically. The currently recommended amount of exercise for older adults is 150 min/week of moderate-intensity exercise; however, the minimum amount of exercise necessary to achieve health benefits is not known. The purpose of this study was to investigate the effects of 12 weeks of participation in a low-volume walking exercise programme (i.e. 90 min/week) combined with daily vitamin E supplementation on thiobarbituric acid reactive substances (TBARS) and oxidised low-density lipoprotein (LDL) concentrations in older adults.
Methods:
The participants were recruited from the following four groups separately: 1) control (CG, n = 14), 2) vitamin E supplementation (SG, n = 10), 3) walking (WG, n = 7), or 4) walking + supplementation (WSG, n = 7). In the CG, participants were advised to maintain their normal lifestyle during the study. Participants in both the SG and WSG received 450 IU (300 mg) /day of alpha-tocopherol for 12 weeks. The exercise programme for the WG and WSG consisted of two 30--60 minute sessions weekly for 12 weeks (average walking time was 44.5 +/- 1.6 min/session). Blood samples were collected at baseline and at 12 weeks.
Results:
Delta plasma oxidised LDL concentrations did not differ among four groups (One-factor ANOVA, P = 0.116). However, negative delta plasma TBARS, a marker of oxidative damage, concentrations were observed in the WG, WSG and SG relative to the CG at the end of the study period (One-factor ANOVA, P = 0.001; post hoc tests; CG compared with WG, WSG and SG, P = 0.005; P = 0.021; P = 0.024, respectively).
Conclusion:
These findings suggest that a low-volume of physical activity and/or vitamin E supplementation may be an effective intervention strategy for reducing TBARS concentrations of older adults.Trial registration: UMIN000008304 (https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&amp;action=brows&amp;type=summary&amp;recptno=R000009782&amp;language=E)</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/38</link>
                <dc:creator>Jong-Hwan Park</dc:creator>
                <dc:creator>Masashi Miyashita</dc:creator>
                <dc:creator>Masaki Takahashi</dc:creator>
                <dc:creator>Noriaki Kawanishi</dc:creator>
                <dc:creator>Seong-Ryu Bae</dc:creator>
                <dc:creator>Hyun-Shik Kim</dc:creator>
                <dc:creator>Katsuhiko Suzuki</dc:creator>
                <dc:creator>Yoshio Nakamura</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:38</dc:source>
        <dc:date>2013-05-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-38</dc:identifier>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/37">
        <title>The silicon supplement `Monomethylsilanetriol&#191; is safe and increases the body pool of silicon in healthy Pre-menopausal women</title>
        <description>Background:
Monomethylsilanetriol (MMST) has been used for decades as an oral silicon supplement for bone and connective tissue health, although there are no formal data on its in vivo utilisation or safety following sustained dosing.
Methods:
To investigate whether MMST contributes to the body pool of silicon and, secondly, to establish its safety following 4 weeks&#8217; supplementation in humans, twenty-two healthy pre-menopausal women (22&#8211;38 years) were recruited and supplemented with MMST at the maximum daily recommended dose (10.5 mg Si/day) for 4 weeks in a double-blind, randomised, placebo-controlled, cross-over design (i.e. 8 weeks in total). Fasting serum and urine samples were collected at baseline and at the end of the 4-week supplementation/placebo periods for analysis of total silicon by inductively coupled plasma optical emission spectrometry, MMST by proton nuclear magnetic resonance spectroscopy and full serum biochemistry. Participants also reported on, by questionnaire, their health, well-being and quality of life at 0, 4 and 8 weeks.
Results:
Overall, 4-weeks supplementation with MMST significantly increased total fasting Si concentrations in serum and urine (P &#8804; 0.003; paired t-test). MMST was semi-quantifiable in serum and quantifiable in urine, but only accounted for ca. 50% and 10%, respectively, of the increased total-Si concentration. There were no reported adverse effects (i.e. changes to health and well-being) or serum biochemical changes with MMST versus placebo.
Conclusions:
Our data indicate that oral MMST is safe, is absorbed and undergoes sufficient metabolism in vivo to raise fasting serum silicon levels, consistent with other well absorbed forms of dietary silicon (e.g. orthosilicic acid). It thus appears to be a suitable silicon supplement.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/37</link>
                <dc:creator>Ravin Jugdaohsingh</dc:creator>
                <dc:creator>Maio Hui</dc:creator>
                <dc:creator>Simon Anderson</dc:creator>
                <dc:creator>Stephen Kinrade</dc:creator>
                <dc:creator>Jonathan Powell</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:37</dc:source>
        <dc:date>2013-04-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-37</dc:identifier>
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        <prism:startingPage>37</prism:startingPage>
        <prism:publicationDate>2013-04-26T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/36">
        <title>Total dietary fat and omega-3 fatty acids have modest effects on urinary sex hormones in postmenopausal women</title>
        <description>Background:
Total fat and omega-3 fatty acids in the diet may affect breast cancer risk by altering estrogen metabolism. The purpose of this study was to elucidate the effects of differing total fat and omega-3 fatty acid content of diets on a panel of urinary estrogens and metabolites.FindingsA controlled, cross-over feeding trial was conducted in postmenopausal women using three test diets: high fat diet (HF; 40% energy from fat), low fat diet (LF; 20% of energy from fat) and low fat, high omega-3 diet (LFn3; 23% energy from fat; 3% omega-3 fatty acids) for 8 week periods. Urinary hormone concentrations for 16 women were compared among diets using a linear mixed model, and within diet comparisons were made using paired t-tests. Urinary excretion of estrone was greater after the LF and LFn3 compared to the HF (P = 0.004). Estrone excretion was increased from baseline within the LF only (P = 0.02). Total estrone + estradiol + estriol increased from baseline with LF (P = 0.02) and was greater than the other two diets at 8 weeks (P = 0.03). There were no effects on estrogen metabolites, including the 2-hydroxy estrone:16&#945;-hydroxy estrone ratio.
Conclusions:
The results of this study indicate that urinary sex hormone metabolism was modestly altered in postmenopausal women by a low fat dietary intervention.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/36</link>
                <dc:creator>Lindsay Young</dc:creator>
                <dc:creator>Susan Raatz</dc:creator>
                <dc:creator>William Thomas</dc:creator>
                <dc:creator>J Redmon</dc:creator>
                <dc:creator>Mindy Kurzer</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:36</dc:source>
        <dc:date>2013-04-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-36</dc:identifier>
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        <prism:startingPage>36</prism:startingPage>
        <prism:publicationDate>2013-04-23T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/35">
        <title>Oral administration of Lactobacillus reuteri GMNL-263 improves insulin resistance and ameliorates hepatic steatosis in high fructose-fed rats</title>
        <description>Background:
Type 2 diabetes mellitus (DM), characterized by peripheral insulin resistance, is the most common form of diabetes. Probiotics are live micro-organisms that, when administered in adequate amounts, confer delaying effect on DM development. In this study, the effects Lactobacillus reuteri GMNL-263 (Lr263), a new probiotic strain developed by our laboratory, on insulin resistance and the development of hepatic steatosis in high-fructose fed rats were explored. Furthermore, the relevant regulatory pathways involved were also investigated.MethodMale Sprague&#8211;Dawley rats were fed a high-fructose diet with or without Lr263 administration for 14 weeks. The composition of fecal microbiota, oral glucose tolerance, glycated haemoglobin, insulin, leptin, C-peptide, and incretins were measured. The markers of liver injury, serum and hepatic lipids profile, activity of hepatic antioxidant enzyme, and proinflammatory cytokines in adipose tissue were investigated. Additionally, the expression of hepatic lipogenic genes and insulin signaling related genes in adipose tissue were also studied. Liver sections were examined for hepatic steatosis using hematoxylin-eosin staining.
Results:
The levels of serum glucose, insulin, leptin, C-peptide, glycated hemoglobin, GLP-1, liver injury markers, lipid profile in serum and liver were significantly increased in high-fructose-fed rats. However, after Lr263 administration, the elevation of these parameters was significantly suppressed. Feeding of Lr263 reversed the decreased number of bifidobacterium species and lactobacillus species and increased number of clostridium species induced by high fructose treatment. The decreased activities of hepatic antioxidant enzymes in HFD rats were dramatically reversed by Lr263 treatment. Concentrations of IL-6 and TNF-&#945; in adipose tissue which were elevated in high fructose treatment were markedly decreased after Lr263 feeding. Decreased levels of PPAR-&#947; and GLUT4 mRNA after high fructose treatment were significantly enhanced by Lr263 administration. Lr263 consumption normalized the increased lipogenic gene (Srebp-1c, FAS, and Elvol6) expressions stimulated by high fructose. Administration of Lr263 significantly ameliorated hepatic steatosis observed in high fructose treated rats.
Conclusion:
Our study provided evidences clarifying the effectiveness of Lr263 on reducing insulin resistance as well as hepatic steatosis formation in high-fructose-fed rats and suggested that Lr263 may be a promising therapeutic agent in treating type 2 diabetes.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/35</link>
                <dc:creator>Feng-Ching Hsieh</dc:creator>
                <dc:creator>Chia-Lin Lee</dc:creator>
                <dc:creator>Chee-Yin Chai</dc:creator>
                <dc:creator>Wan-Tzu Chen</dc:creator>
                <dc:creator>Ying-Chen Lu</dc:creator>
                <dc:creator>Ching-Shuang Wu</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:35</dc:source>
        <dc:date>2013-04-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-35</dc:identifier>
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        <prism:startingPage>35</prism:startingPage>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/34">
        <title>Effects of imiglucerase on the growth and metabolism of Gaucher disease type I patients: a systematic review</title>
        <description>Background:
Gaucher disease (GD) type I is the most common type of GD. Its main clinical manifestations are hepatosplenomegaly as well as bone and hematological abnormalities. The objective of the present study was to perform a literature review on the growth and metabolism of GD type I patients.
Methods:
We searched Pubmed and Scielo.br databases with predetermined study limits: case series (n&#8805;5), clinical trials, systematic reviews, and meta-analyses, and enzyme replacement therapy (ERT) with alglucerase or imiglucerase. The outcomes of interest were the following: growth and development, weight, height, malnutrition, overweight, obesity, basal metabolism, hypermetabolism, insulin resistance, and diabetes. A total of 175 articles were found, of which 28 met the inclusion criteria; these articles were grouped into three central themes: 1) growth of children and adolescents before and after ERT; 2) metabolic changes that remained during ERT; and 3) changes in metabolic status resulting from the treatment.Results and discussionThe articles included in the present literature review are very heterogeneous, which hinders the analysis of data. They indicated that GD patients usually show low weight and height before ERT, which are improved with treatment in children and adolescents. Studies evaluating the energy metabolism by indirect calorimetry have indicated that the disease is associated with hypermetabolism. In adults, some changes in energy metabolism remain on ERT, and alterations, such as insulin resistance, seem to be associated with the treatment. It is not clear which are the required doses of imiglucerase for obtaining an adequate cost-effective relation, as well as the advisable therapeutic measures to avoid possible long-term adverse effects related to ERT.
Conclusions:
ERT tends to normalise the growth of children and adolescents with GD type I, it seems to cause a partial response in relation to some metabolic changes associated with the disease, and it can causes metabolic changes such as weight gain in adult patients. Therefore, additional research is necessary.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/34</link>
                <dc:creator>Divair Doneda</dc:creator>
                <dc:creator>Cristina Netto</dc:creator>
                <dc:creator>Cileide Moulin</dc:creator>
                <dc:creator>Ida Schwartz</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:34</dc:source>
        <dc:date>2013-04-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-34</dc:identifier>
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                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
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        <prism:startingPage>34</prism:startingPage>
        <prism:publicationDate>2013-04-09T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/33">
        <title>Circulating glucagon-like peptide-1 increases in response to short-term overfeeding in men</title>
        <description>Background:
Glucagon-like Peptide-1 (GLP-1) is an incretin hormone secreted from the gastrointestinal tract that facilitates the glucose-dependent insulin response. Additionally, GLP-1 is thought to be involved in energy homeostasis. Currently little is known about GLP-1&#8217;s responsiveness to an energy surplus, a fundamental cause of obesity and diabetes. Our objective was to examine the response of serum GLP-1 to short-term (7&#160;day) overfeeding in young men.
Methods:
Seventy-two young men from the Canadian province of Newfoundland were recruited for the study. For 7-days, the subjects consumed 70% more calories than required at baseline.Various measurements including: anthropometrics, body composition, markers of glucose/lipid metabolism and serum total GLP-1, were taken at a fasted state before (day 1) and after (day 8) the challenge. Paired t-test analyses were used to assess the change in variables after the overfeeding period. Additionally, the relationship between serum GLP-1 and the measured variables at baseline and change due to overfeeding were analyzed.
Results:
Serum GLP-1 was significantly increased in all groups in response to the 7-day energy surplus, indicating the increase was independent of adiposity status. There was no significant difference in fasting GLP-1 at baseline between the normal weight and overweight/obese groups. At baseline, GLP-1 concentration negatively correlated with HDL-cholesterol and positively correlated with triacylglycerols and markers of insulin resistance in the overweight/obese group. Also GLP-1 was negatively correlated with change in percent gynoid fat in the overweight/obese subjects. Percent change in GLP-1 was negatively associated with percent change in gynoid fat in the normal weight group and positively associated with percent change in cholesterol in the overweight/obese group. Percentage change of circulating triacylglycerols was positively associated with percent change in GLP-1 in both adiposity groups.
Conclusion:
Our findings showed that GLP-1 serum concentration is not a significant factor in determining obesity status. The increase of GLP-1 in all subjects regardless of obesity status, suggest GLP-1 serves as a protective role, counteracting energy surplus.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/33</link>
                <dc:creator>Danny Wadden</dc:creator>
                <dc:creator>Farrell Cahill</dc:creator>
                <dc:creator>Peyvand Amini</dc:creator>
                <dc:creator>Edward Randell</dc:creator>
                <dc:creator>Sudesh Vasdev</dc:creator>
                <dc:creator>Yanqing Yi</dc:creator>
                <dc:creator>Jon Church</dc:creator>
                <dc:creator>Guang Sun</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:33</dc:source>
        <dc:date>2013-04-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-33</dc:identifier>
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                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
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        <prism:startingPage>33</prism:startingPage>
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/32">
        <title>Fructose-induced stress signaling in the liver involves methylglyoxal</title>
        <description>Background:
Fructose produces hepatic insulin resistance in humans and animals. We have proposed that the selective metabolism of fructose by the liver can, under conditions of elevated fructose delivery, inflict a metabolic insult that is localized to the hepatocyte. The present study was designed to identify potential cellular effectors of this insult.
Methods:
Primary hepatocytes were incubated with 8&#160;mM glucose and 0.12% inulin (G, n&#8201;=&#8201;6) or 8&#160;mM glucose, 0.12% inulin and 28&#160;mU of inulinase (GF, n&#8201;=&#8201;6) in the presence or absence of insulin for 0, 2, or 4&#160;h.
Results:
GF produced fructose concentrations of ~0.7&#160;mM over the 4&#160;h experiment. GF induced phosphorylation of MKK7 and JNK, phosphorylation of serine307 on IRS-1, and reduced tyrosine phosphorylation of IRS-1 and -2. GF increased ceramide levels and reactive oxygen species (ROS); however inhibitors of ceramide synthesis or ROS accumulation did not prevent GF-mediated changes in MKK7, JNK or IRS proteins. GF increased cellular methylglyoxal concentrations and a selective increase in methylglyoxal recapitulated the GF-induced changes in MKK7, JNK and IRS proteins.
Conclusions:
We hypothesize that GF-mediated changes in stress signaling involve methylglyoxal in primary hepatocytes.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/32</link>
                <dc:creator>Yuren Wei</dc:creator>
                <dc:creator>Dong Wang</dc:creator>
                <dc:creator>Gretchen Moran</dc:creator>
                <dc:creator>Andrea Estrada</dc:creator>
                <dc:creator>Michael Pagliassotti</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:32</dc:source>
        <dc:date>2013-04-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-32</dc:identifier>
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                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>32</prism:startingPage>
        <prism:publicationDate>2013-04-08T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/31">
        <title>A C. elegans model to study human metabolic regulation</title>
        <description>Lipid metabolic disorder is a critical risk factor for metabolic syndrome, triggering debilitating diseases like obesity and diabetes. Both obesity and diabetes are the epicenter of important medical issues, representing a major international public health threat. Accumulation of fat in adipose tissue, muscles and liver and/or the defects in their ability to metabolize fatty acids, results in insulin resistance. This triggers an early pathogenesis of type 2 diabetes (T2D). In mammals, lipid metabolism involves several organs, including the brain, adipose tissue, muscles, liver, and gut. These organs are part of complex homeostatic system and communicate through hormones, neurons and metabolites. Our study dissects the importance of mammalian Kr&#252;ppel-like factors in over all energy homeostasis. Factors controlling energy metabolism are conserved between mammals and Caenorhabditis elegans providing a new and powerful strategy to delineate the molecular pathways that lead to metabolic disorder. The C. elegans intestine is our model system where genetics, molecular biology, and cell biology are used to identify and understand genes required in fat metabolism. Thus far, we have found an important role of C. elegans KLF in FA biosynthesis, mitochondrial proliferation, lipid secretion, and &#946;-oxidation. The mechanism by which KLF controls these events in lipid metabolism is unknown. We have recently observed that C. elegans KLF-3 selectively acts on insulin components to regulate insulin pathway activity. There are many factors that control energy homeostasis and defects in this control system are implicated in the pathogenesis of human obesity and diabetes. In this review we are discussing a role of KLF in human metabolic regulation.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/31</link>
                <dc:creator>Sarwar Hashmi</dc:creator>
                <dc:creator>Yi Wang</dc:creator>
                <dc:creator>Ranjit Parhar</dc:creator>
                <dc:creator>Kate Collison</dc:creator>
                <dc:creator>Walter Conca</dc:creator>
                <dc:creator>Futwan Al-Mohanna</dc:creator>
                <dc:creator>Randy Gaugler</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:31</dc:source>
        <dc:date>2013-04-04T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-31</dc:identifier>
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                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>31</prism:startingPage>
        <prism:publicationDate>2013-04-04T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.nutritionandmetabolism.com/content/10/1/29">
        <title>Caloric restriction favorably impacts metabolic and immune/inflammatory profiles in obese mice but curcumin/piperine consumption adds no further benefit</title>
        <description>Background:
Obesity is associated with low-grade inflammation and impaired immune response. Caloric restriction (CR) has been shown to inhibit inflammatory response and enhance cell-mediated immune function. Curcumin, the bioactive phenolic component of turmeric spice, is proposed to have anti-obesity and anti-inflammation properties while piperine, another bioactive phenolic compound present in pepper spice, can enhance the bioavailability and efficacy of curcumin. This study sought to determine if curcumin could potentiate CR&#8217;s beneficial effect on immune and inflammatory responses in obesity developed in mice by feeding high-fat diet (HFD).
Methods:
Mice were fed a HFD for 22 wk and then randomized into 5 groups: one group remained on HFD ad libitum and the remaining 4 groups were fed a 10% CR (reduced intake of HFD by 10% but maintaining the same levels of micronutrients) in the presence or absence of curcumin and/or piperine for 5 wk, after which CR was increased to 20% for an additional 33 wk. At the end of the study, mice were sacrificed, and spleen cells were isolated. Cells were stimulated with T cell mitogens, anti-CD3/CD28 antibodies, or lipopolysaccharide to determine T cell proliferation, cytokine production, and CD4+ T cell subpopulations.
Results:
Compared to HFD control group, all CR mice, regardless of the presence of curcumin and/or piperine, had lower body weight and fat mass, lower levels of blood glucose and insulin, and fewer total spleen cells but a higher percentage of CD4+ T cells. Additionally, they demonstrated lower production of pro-inflammatory cytokines IL-1&#946; and TNF-&#945;, a trend toward lower IL-6, and lower production of PGE2, a lipid molecule with pro-inflammatory and T cell-suppressive properties. Mice with CR alone had higher splenocyte proliferation and IL-2 production, but this effect of CR was diminished by spice supplementation. CR alone or in combination with spice supplementation had no effect on production of cytokines IL-4, IL-10, IFN-&#947;, and IL-17, or the proportion of different CD4+ T cell subsets.
Conclusion:
CR on an HFD favorably impacts both metabolic and immune/inflammatory profiles; however, the presence of curcumin and/or piperine does not amplify CR&#8217;s beneficial effects.</description>
        <link>http://www.nutritionandmetabolism.com/content/10/1/29</link>
                <dc:creator>Junpeng Wang</dc:creator>
                <dc:creator>Sally Vanegas</dc:creator>
                <dc:creator>Xiaogang Du</dc:creator>
                <dc:creator>Timothy Noble</dc:creator>
                <dc:creator>Jean-Marc Zingg</dc:creator>
                <dc:creator>Mohsen Meydani</dc:creator>
                <dc:creator>Simin Meydani</dc:creator>
                <dc:creator>Dayong Wu</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2013, null:29</dc:source>
        <dc:date>2013-03-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-10-29</dc:identifier>
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                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
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        <prism:startingPage>29</prism:startingPage>
        <prism:publicationDate>2013-03-27T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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