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 Nutrition, Metabolism &amp; Cardiovascular Diseases  is a forum designed to focus on the powerful 
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   </description><link>http://www.nmcd-journal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:issn>0939-4753</prism:issn><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:publicationDate>June 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475312001068/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002188/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475312000567/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310001900/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310001870/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002103/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002164/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002218/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002176/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002206/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475310002474/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475312001068/abstract?rss=yes"><title>Editorial Board</title><link>http://www.nmcd-journal.com/article/PIIS0939475312001068/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0939-4753(12)00106-8</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002188/abstract?rss=yes"><title>Effect of soy isoflavones on blood pressure: A meta-analysis of randomized controlled trials</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002188/abstract?rss=yes</link><description>Abstract: Background and aim: The effect of soy isoflavones on blood pressure is controversial. The objective of this study was to evaluate the effect of dietary soy isoflavones on blood pressure.Methods and Results: Trials were searched in PubMed, the Cochrane Library, Embase and references cited in related reviews and studies. A total of eleven trials were reviewed. Meta-analysis results showed a mean decrease of 2.5 mm Hg (95% CIs, − 5.35 to 0.34 mm Hg; P = 0.08) for systolic blood pressure and 1.5 mm Hg (95% CIs, − 3.09 to 0.17 mm Hg; P = 0.08) for diastolic blood pressure in the soy isoflavones-treated group compared to placebo. Meta-regression and subgroup analyses indicated that blood pressure status was a significant predictor of heterogeneity for the effect of soy isoflavones on blood pressure. Subgroup analysis of hypertensive subjects revealed that a greater blood pressure reduction was identified in the soy isoflavone-treated group compared to placebo (5 trials; SBP: − 5.94, 95% CIs [− 10.55, − 1.34] mm Hg, P = 0.01; DBP: − 3.35, 95% CIs [- 6.52, − 0.19] mm Hg, P = 0.04). In contrast, treatment with soy isoflavones did not lead to a significant reduction in blood pressure in normotensive subjects (6 trials; SBP: 0.29, 95% CIs [- 2.39, 2.97] mm Hg, P = 0.83; DBP: − 0.43, 95% CIs [- 1.66, 0.81] mm Hg, P = 0.50).Conclusion: Soy isoflavones had an effect of lowering blood pressure in hypertensive subjects, but not in normotensive subjects. Larger trials need to be carried out to confirm the present findings.</description><dc:title>Effect of soy isoflavones on blood pressure: A meta-analysis of randomized controlled trials</dc:title><dc:creator>X.X. Liu, S.H. Li, J.Z. Chen, K. Sun, X.J. Wang, X.G. Wang, R.T. Hui</dc:creator><dc:identifier>10.1016/j.numecd.2010.09.006</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2011-02-10</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2011-02-10</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Systematic Reviews and Meta-analyses</prism:section><prism:startingPage>463</prism:startingPage><prism:endingPage>470</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475312000567/abstract?rss=yes"><title>Gut–liver axis: The impact of gut microbiota on non alcoholic fatty liver disease</title><link>http://www.nmcd-journal.com/article/PIIS0939475312000567/abstract?rss=yes</link><description>Abstract: Aim: To examine the impact of gut microbiota on non alcoholic fatty liver disease (NAFLD) pathogenesis.Data synthesis: Emerging evidence suggests a strong interaction between gut microbiota and liver. Receiving approximately 70% of its blood supply from the intestine, the liver represents the first line of defence against gut-derived antigens. Intestinal bacteria play a key role in the maintenance of gut–liver axis health. Disturbances in the homeostasis between bacteria- and host-derived signals at the epithelial level lead to a break in intestinal barrier function and may foster “bacterial translocation”, defined as the migration of bacteria or bacterial products from the intestinal lumen to mesenteric lymph nodes or other extraintestinal organs and sites. While the full repertoire of gut-derived microbial products that reach the liver in health and disease has yet to be explored, the levels of bacterial lipopolysaccharide, a component of the outer membrane of Gram-negative bacteria, are increased in the portal and/or systemic circulation in several types of chronic liver diseases. Derangement of the gut flora, particularly small intestinal bacterial overgrowth, occurs in a large percentage (20–75%) of patients with chronic liver disease. In addition, evidence implicating the gut–liver axis in the pathogenesis of metabolic liver disorders has accumulated over the past ten years.Conclusions: Complex metabolic diseases are the product of multiple perturbations under the influence of triggering factors such as gut microbiota and diet, thus, modulation of the gut microbiota may represent a new way to treat or prevent NAFLD.</description><dc:title>Gut–liver axis: The impact of gut microbiota on non alcoholic fatty liver disease</dc:title><dc:creator>D. Compare, P. Coccoli, A. Rocco, O.M. Nardone, S. De Maria, M. Cartenì, G. Nardone</dc:creator><dc:identifier>10.1016/j.numecd.2012.02.007</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2012-04-30</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2012-04-30</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>471</prism:startingPage><prism:endingPage>476</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310001900/abstract?rss=yes"><title>A derangement of the maternal lipid profile is associated with an elevated risk of congenital heart disease in the offspring</title><link>http://www.nmcd-journal.com/article/PIIS0939475310001900/abstract?rss=yes</link><description>Abstract: Background and aims: Maternal hyperglycaemia and hyperhomocysteinaemia are risk factors for congenital heart disease (CHD). These metabolic derangements and deranged lipid levels are associated with adult cardiovascular disease. We examined whether maternal lipid levels are associated with the risk of CHD offspring.Methods and Results: From 2003 onwards, a case-control study was conducted. Participants were mothers of children with (n = 261) and without (n = 325) CHD. At around 16 months after the index-pregnancy, maternal lipid levels were determined. Maternal characteristics and lipid levels were compared by Student’s t-test. In a multivariable logistic regression model, risk estimates were calculated for associations between CHD and lipid levels. Adjustments were made for maternal age, diabetes, ethnicity, body mass index (BMI), parity, periconception folic acid use and total homocysteine levels. Outcome measures are presented in (geometric) means (p5–p95) and odds ratios (ORs) with 95% confidence intervals (CIs).Case mothers showed higher cholesterol (4.9 vs. 4.7 mmol l−1, P &lt; 0.05), low-density lipoprotein (LDL)-cholesterol (3.2 vs. 3.0 mmol l−1, P &lt; 0.05), apolipoprotein B (84.0 vs. 80.0 mg dl−1, P &lt; 0.01) and homocysteine (10.8 vs. 10.2 μmol l−1, P &lt; 0.05) than controls. LDL-cholesterol above 3.3 mmol l−1 (OR 1.6 (95%CI, 1.1–2.3)) and apolipoprotein B above 85.0 mg dl−1 were associated with an almost twofold increased CHD risk (OR 1.8 (95%CI, 1.2–2.6)). This was supported by elevated CHD risks per unit standard deviation increase in cholesterol (OR 1.2 (95% CI 1.03–1.5)), LDL-cholesterol (OR 1.3 (95%CI, 1.1–1.6) and apolipoprotein B (OR 1.3 (95% CI 1.1–1.6)). Apolipoprotein B was most strongly associated with CHD risk.Conclusion: A mildly deranged maternal lipid profile is associated with an increased risk of CHD offspring.</description><dc:title>A derangement of the maternal lipid profile is associated with an elevated risk of congenital heart disease in the offspring</dc:title><dc:creator>H.P.M. Smedts, E.M. van Uitert, O. Valkenburg, J.S.E. Laven, M.J.C. Eijkemans, J. Lindemans, E.A.P. Steegers, R.P.M. Steegers-Theunissen</dc:creator><dc:identifier>10.1016/j.numecd.2010.07.016</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2010-12-27</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-12-27</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>477</prism:startingPage><prism:endingPage>485</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310001870/abstract?rss=yes"><title>Receptor identification and physiological characterisation of glucagon-like peptide-2 in the rat heart</title><link>http://www.nmcd-journal.com/article/PIIS0939475310001870/abstract?rss=yes</link><description>Abstract: Background and aims: The anorexigenic glucagon-like peptide (GLP)-2 is produced by intestinal L cells and released in response to food intake. It affects intestinal function involving G-protein-coupled receptors. To verify whether GLP-2 acts as a cardiac modulator in mammals, we analysed, in the rat heart, the expression of GLP-2 receptors and the myocardial and coronary responses to GLP-2.Methods and results: GLP-2 receptors were detected on ventricular extracts by quantitative real-time polymerase chain reaction (Q-RT-PCR) and Western blotting. Cardiac GLP-2 effects were analysed on Langendorff perfused hearts. Intracellular GLP-2 signalling was investigated on Langendorff perfused hearts and by Western blotting and enzyme-linked immunosorbent assay (ELISA) on ventricular extracts.By immunoblotting and Q-RT-PCR, we revealed the expression of ventricular GLP-2 receptors. Perfusion analyses showed that GLP-2 induces positive inotropism at low concentration (10–12 mol l−1), and negative inotropism and lusitropism from 10 to 10 mol l−1. It dose-dependently constricts coronaries. The negative effects of GLP-2 were independent from GLP-1 receptors, being unaffected by exendin-3 (9–39) amide. GLP-2-dependent negative action involves Gi/o proteins, associates with a reduction of intracellular cyclic adenosine monophosphate (cAMP), an increase in extracellular signal regulated kinases 1 and 2 (ERK1/2) and a decrease in phospholamban phosphorylation, but is independent from endothelial nitric oxide synthase (eNOS) and protein kinase G (PKG). Finally, GLP-2 competitively antagonised β-adrenergic stimulation.Conclusions: For the first time, to our knowledge, we found that: (1) the rat heart expresses functional GLP-2 receptors; (2) GLP-2 acts on both myocardium and coronaries, negatively modulating both basal and β-adrenergic stimulated cardiac performance; and (3) GLP-2 effects are mediated by G-proteins and involve ERK1/2.</description><dc:title>Receptor identification and physiological characterisation of glucagon-like peptide-2 in the rat heart</dc:title><dc:creator>T. Angelone, E. Filice, A.M. Quintieri, S. Imbrogno, N. Amodio, T. Pasqua, D. Pellegrino, F. Mulè, M.C. Cerra</dc:creator><dc:identifier>10.1016/j.numecd.2010.07.014</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2010-12-27</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-12-27</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>486</prism:startingPage><prism:endingPage>494</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002103/abstract?rss=yes"><title>The beta-1 adrenergic antagonist, atenolol, decreases acylation stimulating protein, exercise capacity and plasma free fatty acids in men with type 2 diabetes</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002103/abstract?rss=yes</link><description>Abstract: Background and aims: Atenolol is a beta-1 adrenergic antagonist commonly prescribed for the treatment of systemic hypertension or coronary artery disease yet its use in individuals with type 2 diabetes mellitus (T2DM) is controversial due to potentially negative side effects on insulin resistance. Non-esterified fatty acid (NEFA) metabolism is altered in T2DM especially under conditions of metabolic stress such as exercise or the postprandial state. We evaluated atenolol effects on circulating NEFA and related hormones in men with T2DM during acute cardiorespiratory exercise in both the fasting and postprandial state, including the adipokine acylation stimulating protein (ASP) which stimulates adipose tissue NEFA uptake.Methods and results: Ten men with T2DM underwent four 1-h exercise sessions at 60% of their maximal oxygen uptake (VO2max) under the following conditions: 1) fasting (F), and 2) 2 h postprandial (PP) without medication; and 3) fasting (F-Atenolol), and 4) 2 h postprandial (PP-Atenolol) after a one-week treatment with atenolol. Results were tested for the effects of atenolol via two-way ANOVA for the F vs F-Atenolol and PP vs PP-Atenolol states separately. Atenolol treatment decreased fasting and postprandial glycerol (p &lt; 0.0001) and NEFA (p &lt; 0.0001), postprandial epinephrine (p = 0.048), postprandial cortisol (p = 0.02), postprandial ASP (p = 0.04) and postprandial dopamine (p &lt; 0.004).Conclusion: Atenolol alters fatty acid metabolism and associated metabolic hormones including ASP during exercise in men with T2DM and its effects are more apparent during conditions of stress such as the postprandial state, acute exercise and obesity.</description><dc:title>The beta-1 adrenergic antagonist, atenolol, decreases acylation stimulating protein, exercise capacity and plasma free fatty acids in men with type 2 diabetes</dc:title><dc:creator>J. Smith, A. Ferland, J. Méthot, P. Brassard, S. Lacroix, P. Poirier, K. Cianflone</dc:creator><dc:identifier>10.1016/j.numecd.2010.08.008</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2011-01-20</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2011-01-20</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>495</prism:startingPage><prism:endingPage>502</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002164/abstract?rss=yes"><title>Genetic and environmental relationships between Framingham Risk Score and adiposity measures in Koreans: The Healthy Twin Study</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002164/abstract?rss=yes</link><description>Abstract: Background and aims: We examined heritability and bivariate analyses for the Framingham Risk Score (FRS) and adiposity measures among Koreans.Methods and results: We analysed the data from 2496 participants (962 men, 1534 women, age 30–74 years), including 1320 non-twin family members, 468 monozygotic (MZ) and 120 dizygotic (DZ) twin pairs, collected from the Healthy Twin study of Korea. Adiposity measurements comprised BMI, waist circumference (WC), waist-to-hip ratio and waist-to-height ratio (WHTR). Analyses were conducted using the Sequential Oligogenic Linkage Analysis Routines (SOLAR) package software. The co-twin control analyses shows that estimates of within-pair regression coefficients in the relationship between adiposity traits and FRS were attenuated for MZ twin pairs, relative to DZ twin pairs (0.11–0.26 vs. 0.60–0.71). The heritability estimate for FRS was 0.37, and the estimates for adiposity traits ranged from 0.45 to 0.63 (P   0.05) to 0.46 (for WC, P &lt; 0.001). The common environmental correlations between FRS and each of the adiposity traits ranged from 0.43 to 0.66 (P &lt; 0.001).Conclusions: FRS and each of the obesity traits shared common genetic and environmental relationships. These findings support a pleiotropic action between genes associated with adiposity traits and FRS and a need of further investigations for identifying specific common environmental factors.</description><dc:title>Genetic and environmental relationships between Framingham Risk Score and adiposity measures in Koreans: The Healthy Twin Study</dc:title><dc:creator>Y. Song, K. Lee, J. Sung, D. Lee, M.K. Lee, J.Y. Lee</dc:creator><dc:identifier>10.1016/j.numecd.2010.09.004</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2010-12-27</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-12-27</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>503</prism:startingPage><prism:endingPage>509</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002218/abstract?rss=yes"><title>Metabolic syndrome and coronary heart disease among Spanish male workers: A case-control study of MESYAS</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002218/abstract?rss=yes</link><description>Abstract: Background and aims: In Spain, the incidence of coronary heart disease is below that expected based on the burden of classic cardiovascular risk factors present in the population. Whether the risk associated with metabolic syndrome is lower in Spain deserves to be investigated. This study evaluates the association of incident clinical coronary heart disease with metabolic syndrome and each of its individual defining components in a sample of Spanish working males.Methods and results: Among the workers of a factory (MESYAS registry), 208 incident cases of coronary heart disease (between 1981 and 2005) were age-matched with 2080 healthy workers visited in 2004–2005. Metabolic syndrome was characterized using modified criteria of the joint consensus definition (2009). Metabolic syndrome was strongly associated with coronary heart disease (OR = 4.03; 95% CI: 2.98, 5.45) and the risk seemed to be fully explained by metabolic syndrome components (OR = 0.84, p = 0.54 after adjustment). Odds ratios for the independent effects of the diagnostic criteria were: hypertriglyceridemia (OR = 3.39, p &lt; 0.001), hyperglycemia (OR = 2.70, p &lt; 0.001), low HDL cholesterol (OR = 2.35, p &lt; 0.001), hypertension (OR = 1.49, p = 0.016) and overweight (OR = 1.07, p = 0.678). Young workers showed a higher risk associated with metabolic syndrome.Conclusion: The risk associated with metabolic syndrome is fully explained by its components considered independently. The risk of coronary heart disease in a Spanish male working population is considerably increased among those with metabolic syndrome, by a factor similar to that described for other countries. Public health measures to prevent a rise in the prevalence of metabolic syndrome are advisable to minimize cardiovascular disease rate in Spain.</description><dc:title>Metabolic syndrome and coronary heart disease among Spanish male workers: A case-control study of MESYAS</dc:title><dc:creator>M. Laclaustra, B. Ordoñez, M. Leon, E.M. Andres, A. Cordero, I. Pascual-Calleja, A. Grima, E. Luengo, E. Alegria, M. Pocovi, F. Civeira, J.A. Casasnovas-Lenguas</dc:creator><dc:identifier>10.1016/j.numecd.2010.09.009</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2010-12-27</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-12-27</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>510</prism:startingPage><prism:endingPage>516</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002176/abstract?rss=yes"><title>Gender differences in copper, zinc and selenium status in diabetic-free metabolic syndrome European population – The IMMIDIET study</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002176/abstract?rss=yes</link><description>Abstract: Background and aims: The European ‘IMMIDIET’ study was designed to evaluate the effect of genetic and dietary habit interactions on cardiovascular disease risk factors in non-diabetic subjects. Copper, zinc and selenium are involved in redox balance and modifications of their homeostasis could be associated with metabolic syndrome. Because few studies have dealt with trace element status in metabolic syndrome with conflicting results, we aimed at investigating the relationships between plasma copper, zinc and selenium concentrations and metabolic syndrome in the IMMIDIET population.Methods and results: Male–female couples born and living in Abruzzo, Italy (n = 271); Limburg, Belgium (n = 267), southwest part of London, England (n = 263) and 205 Italian–Belgian mixed couples living in Belgium were enrolled. Data on medical history, hypertension and blood lipid profile, medication use, smoking and alcohol habits, physical activity and socioeconomic status were collected using a standardised questionnaire. Anthropometric, blood pressure, glucose, insulin, lipid profile and copper, zinc and selenium measurements were performed. Participants were classified in two groups according to the presence of metabolic syndrome (Yes/No).Comparison between these two groups, performed separately in men and women, indicated no association in men whereas, in women, metabolic syndrome was associated with higher plasma selenium concentrations (odds ratio (OR) = 1.55(1.28–1.89)); this association remained significant after adjustment for age, group, social status, physical activity, energy intake, alcohol consumption, smoking and hormonal status (OR = 1.33 (1.06–1.67)).Conclusion: Our results indicate gender differences in the association between plasma selenium concentration and metabolic syndrome without diabetes and may suggest a sub-clinical deleterious effect of high selenium status in women.</description><dc:title>Gender differences in copper, zinc and selenium status in diabetic-free metabolic syndrome European population – The IMMIDIET study</dc:title><dc:creator>J. Arnaud, M. de Lorgeril, T. Akbaraly, P. Salen, J. Arnout, F.P. Cappuccio, M.C.J.M. van Dongen, M.B. Donati, V. Krogh, A. Siani, L. Iacoviello, on behalf of the European Collaborative Group of the IMMIDIET Project</dc:creator><dc:identifier>10.1016/j.numecd.2010.09.005</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2011-01-03</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2011-01-03</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>517</prism:startingPage><prism:endingPage>524</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002206/abstract?rss=yes"><title>The role of serum adipocyte fatty acid-binding protein on the development of metabolic syndrome is independent of pro-inflammatory cytokines</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002206/abstract?rss=yes</link><description>Abstract: Background and aim: Adipocyte fatty acid-binding protein (FABP4) is abundantly expressed in adipocytes and plays a role in glucose homeostasis. We analysed the relationship between serum FABP4 levels and the progression of metabolic syndrome in healthy adults.Methodsand results: A total of 465 subjects were selected from participants in a medical check-up programme at a Health Promotion Center. Baseline serum FABP4 levels were measured, and the subjects were evaluated for the presence of metabolic syndrome (MetS) according to the recommendations of the American Heart Association/National Heart, Lung, and Blood Institute. The subjects were re-evaluated 4 years later.Baseline FABP4 concentrations were significantly higher in subjects with MetS than in those without MetS (P&lt;0.001). At the 4-year follow-up, subjects in the highest FABP4 tertile at baseline exhibited higher values for body mass index, fat mass and percent body fat, as well as blood pressure, fasting glucose, total cholesterol, triglycerides, low-density lipoprotein (LDL)-cholesterol, insulin, homeostasis model assessment of insulin resistance, monocyte chemoattractant protein-1 and tumor necrosis factor-α levels (all P&lt;0.05). The subjects with higher FABP4 levels had lower HDL-cholesterol concentrations (P&lt;0.05). After adjustment for age, sex, change in percent body fat and baseline values for other metabolic and inflammatory parameters, FABP4 levels at baseline were shown to be strongly associated with the development of MetS by year 4 (odds ratio (OR), 5.75; 95% confidence interval (CI), 2.71–12.23 for highest tertile vs. lowest tertile, P&lt;0.001)Conclusion: Baseline serum FABP4 levels appear to be a significant predictor for the future development of MetS, independent of pro-inflammatory cytokines.</description><dc:title>The role of serum adipocyte fatty acid-binding protein on the development of metabolic syndrome is independent of pro-inflammatory cytokines</dc:title><dc:creator>S.E. Park, E.-J. Rhee, W.-Y. Lee, W.-J. Kim, S.-H. Yoo, J.-C. Bae, E.-S. Choi, C.-Y. Park, K.-W. Oh, S.-W. Park, S.-W. Kim</dc:creator><dc:identifier>10.1016/j.numecd.2010.09.008</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2010-12-27</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-12-27</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>525</prism:startingPage><prism:endingPage>532</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310002474/abstract?rss=yes"><title>Birth weight, current body mass index, and insulin sensitivity and secretion in young adults in two Latin American populations</title><link>http://www.nmcd-journal.com/article/PIIS0939475310002474/abstract?rss=yes</link><description>Abstract: Background and aims: Although studies have shown association of birth weight (BW) and adult body mass index (BMI) with insulin sensitivity in adults, there is limited evidence that BW is associated with insulin secretion. We assessed the associations between BW and current BMI with insulin sensitivity and secretion in young Latin American adults.Methods and results: Two birth cohorts, one from Ribeirao Preto, Brazil, based on 1984 participants aged 23–25 years, and another from Limache, Chile, based on 965 participants aged 22–28 years were studied. Weight and height at birth, and current fasting plasma glucose and insulin levels were measured. Insulin sensitivity (HOMA%S) and secretion (HOMA%β) were estimated using the Homeostatic Model Assessment (HOMA2). Multiple linear regression analyses were carried out to test the associations between BW and adult BMI z-scores on log HOMA%S and log HOMA%β. BW z-score was associated with HOMA%S in the two populations and HOMA%β in Ribeirao Preto when adult BMI z-score was included in the model. BW z-score was associated with decreasing insulin secretion even without adjusting for adult BMI, but only in Ribeirao Preto. BMI z-score was associated with low HOMA%S and high HOMA%β. No interactions between BW and BMI z-scores on insulin sensitivity were shown.Conclusions: This study supports the finding that BW may affect insulin sensitivity and secretion in young adults. The effect size of BW on insulin status is small in comparison to current BMI.</description><dc:title>Birth weight, current body mass index, and insulin sensitivity and secretion in young adults in two Latin American populations</dc:title><dc:creator>A.A.M. Silva, C.J.N. Santos, H. Amigo, M.A. Barbieri, P. Bustos, H. Bettiol, R.J. Rona</dc:creator><dc:identifier>10.1016/j.numecd.2010.09.012</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 22, 6 (2012)</dc:source><dc:date>2011-05-05</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2011-05-05</prism:publicationDate><prism:volume>22</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0939-4753(12)X0006-1</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>533</prism:startingPage><prism:endingPage>539</prism:endingPage></item></rdf:RDF>
