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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.nmcd-journal.com/?rss=yes"><title>Nutrition, Metabolism &amp; Cardiovascular Diseases</title><description>Nutrition, Metabolism &amp; Cardiovascular Diseases RSS feed: Current Issue. 
 Nutrition, Metabolism &amp; Cardiovascular Diseases  is a forum designed to focus on the powerful interplay between nutritional 
and metabolic alterations, and cardiovascular disorders. It aims to be a highly qualified tool to help refine strategies against the 
nutrition-related epidemics of metabolic and cardiovascular diseases. By presenting original clinical and experimental findings, it introduces 
readers and authors into a rapidly developing area of clinical and preventive medicine, including also vascular biology. Of particular 
concern are the origins, the mechanisms and the means to prevent and control diabetes, atherosclerosis, hypertension, and other nutrition-related 
diseases. 
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2008 and March 2009 
</description><link>http://www.nmcd-journal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 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>20</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2010</prism:publicationDate><prism:copyright> © 2009 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/PIIS0939475310000220/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309001859/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000593/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000635/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000623/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000453/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000660/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000581/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309000659/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309001896/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309001197/abstract?rss=yes"/><rdf:li rdf:resource="http://www.nmcd-journal.com/article/PIIS0939475309001215/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475310000220/abstract?rss=yes"><title>Editorial Board</title><link>http://www.nmcd-journal.com/article/PIIS0939475310000220/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0939-4753(10)00022-0</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</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/PIIS0939475309001859/abstract?rss=yes"><title>Measuring and estimating insulin resistance in clinical and research settings</title><link>http://www.nmcd-journal.com/article/PIIS0939475309001859/abstract?rss=yes</link><description>Abstract: Aim: This short review provides a theoretical outline for the measurement of insulin secretion and insulin resistance in humans.Data synthesis: To evaluate the ability to secrete insulin, disposition index must be considered, and it is necessary to assess insulin sensitivity when insulin secretion is induced for assessment. The clinical application of the measurement of insulin resistance is also introduced for further debate. The term “insulin effectiveness” is clinical jargon for insulin sensitivity. However, for clinical application, you need at least two types of insulin effectiveness to calculate a basal and bolus insulin administration dose, while peripheral (mainly muscle) and liver are two major target organs for insulin action. The term “insulin sensitivity” may be used to express insulin action of the muscle or of specific organs through their insulin receptors, while “insulin resistance” may be used to express the necessity of a dose of insulin administration to suppress hepatic glucose production that can be induced by substrates, glucagon, catecholamine, and so on.Conclusions: This article covers several important issues on the measurement of insulin secretion and resistance that had not been well described in other review articles, and may be of help for future clinical investigation.</description><dc:title>Measuring and estimating insulin resistance in clinical and research settings</dc:title><dc:creator>M. Matsuda</dc:creator><dc:identifier>10.1016/j.numecd.2009.07.007</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-10-12</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-10-12</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Viewpoint</prism:section><prism:startingPage>79</prism:startingPage><prism:endingPage>86</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000593/abstract?rss=yes"><title>Lifestyle intervention improves microvascular reactivity and increases serum adiponectin in overweight hypertensive patients</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000593/abstract?rss=yes</link><description>Abstract: Background and aims: Obesity and hypoadiponectinemia are often associated with high blood pressure. Moreover, microvascular dysfunction is reported to be an early event in patients with hypertension and may be involved in the pathogenesis of organ damage.Methods and results: We investigated the impact of 8-week moderate-intensity aerobic training on adiponectin plasma levels and skin microvascular reactivity in 24 overweight sedentary patients (18 men, age 44±6 years, body mass index 28±3kg/m2) with never-treated grade 1 essential hypertension. Twenty-four age- and sex-matched hypertensive patients, who were examined twice at 8-week intervals in the absence of exercise training, served as controls. Exercise training was followed by a significant reduction in waist circumference (from 97±9 to 95±9cm, p&lt;0.05) and an increase in adiponectin plasma levels (from 11.9±3 to 12.5±4mg/L, p&lt;0.05). An inverse correlation was found between adiponectin change and waist circumference change (r=−0.43, p&lt;0.05). The area under the curve after post-occlusive reactive hyperemia at skin laser-Doppler examination increased significantly after aerobic training (from 876±539 to 1468±925PU/s, p&lt;0.001). A positive correlation was found between exercise-induced variations of post-occlusive reactive hyperemia and adiponectin plasma levels (r=0.41, p&lt;0.05). Office or 24-h blood pressure values did not change significantly.Conclusion: In sedentary overweight patients with mild hypertension, moderate aerobic training improves cutaneous microvascular reactivity and adiponectin plasma levels. These changes precede blood pressure reduction and may serve as biomarkers of the efficacy of non-drug treatment in hypertensive patients.</description><dc:title>Lifestyle intervention improves microvascular reactivity and increases serum adiponectin in overweight hypertensive patients</dc:title><dc:creator>L. Pasqualini, G. Schillaci, S. Innocente, G. Pucci, F. Coscia, D. Siepi, G. Lupattelli, G. Ciuffetti, E. Mannarino</dc:creator><dc:identifier>10.1016/j.numecd.2009.03.002</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-05-28</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-05-28</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>87</prism:startingPage><prism:endingPage>92</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000635/abstract?rss=yes"><title>Metabolic syndrome in primary aldosteronism and essential hypertension: Relationship to adiponectin gene variants</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000635/abstract?rss=yes</link><description>Abstract: Background and aims: Evidence shows that aldosterone excess is crucial for the development of cardiac and metabolic complications. Among the possible pathogenetic elements of the metabolic syndrome, adiponectin and its polymorphisms seem to confer a genetic risk for metabolic alterations and type 2 diabetes.Aims of the study were to investigate whether metabolic syndrome represents a common feature in patients with primary aldosteronism (PA) compared with essential hypertensives (EH) and to study the impact of two common adiponectin gene variants on the parameters of metabolic syndrome.Methods and results: Metabolic syndrome was defined according to ATPIII criteria. Eighty-nine patients with PA and 164 matched EH were studied. In all patients with PA and in 135 EH two single nucleotide polymorphisms of the adiponectin gene, T45G and G276T, were detected. Patients with PA displayed a higher prevalence of metabolic syndrome compared with EH (45% vs. 30%, p&lt;0.05). In patients with PA, genotypes 45T/G+G/G were associated with significantly lower values of waist circumference, HOMA-IR and serum aldosterone. In both PA patients and EH, the 276T/T genotype was associated with significantly worse metabolic profile and a higher risk for the metabolic syndrome (OR=1.5 for PA and OR=1.3 for EH).Conclusions: Our data confirm a higher prevalence of metabolic syndrome among patients with PA compared with matched EH. Genetic analysis of T45G and G276T adiponectin gene polymorphisms showed that, while the genotypes 45G/G+G/T seemed to have a protective role on the metabolic complications, the genotype 276T/T defined PA and EH patients with a worse metabolic profile.</description><dc:title>Metabolic syndrome in primary aldosteronism and essential hypertension: Relationship to adiponectin gene variants</dc:title><dc:creator>V. Ronconi, F. Turchi, S. Rilli, D. Di Mattia, L. Agostinelli, M. Boscaro, G. Giacchetti</dc:creator><dc:identifier>10.1016/j.numecd.2009.03.007</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-06-01</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-06-01</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>93</prism:startingPage><prism:endingPage>100</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000623/abstract?rss=yes"><title>Acute effects of casein on postprandial lipemia and incretin responses in type 2 diabetic subjects</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000623/abstract?rss=yes</link><description>Abstract: Background and aims: Exaggerated and prolonged postprandial lipemia is potentially atherogenic and associated with type 2 diabetes. Limited data exist regarding the influence of dietary protein on postprandial lipemia in type 2 diabetes. We investigated, over 8-h, the acute effects of casein alone or in combination with carbohydrate on postprandial lipid and incretin responses to a fat-rich meal in type 2 diabetes.Methods and results: Eleven type 2 diabetic subjects ingested four test meals in random order: an energy-free soup plus 80g of fat (control-meal); control-meal plus 45g carbohydrates (CHO-meal); control-meal plus 45g of casein (PRO-meal); and PRO-meal plus 45g carbohydrates (CHO+PRO-meal). Triglyceride and retinyl palmitate responses were measured in plasma and in a chylomicron-rich and chylomicron-poor fraction. We found no significant differences in triglyceride responses to PRO- and CHO+PRO-meal compared to the control-meal. However, the addition of casein to the CHO-meal reduced the raised triglyceride response in the chylomicron-rich fraction. Retinyl palmitate responses did not differ significantly between meals in the chylomicron-rich fraction, whereas the PRO-meal increased retinyl palmitate in the chylomicron-poor fraction. PRO- and PRO+CHO-meal increased insulin and glucagon compared to the control-meal. PRO+CHO-meal increased the glucose-dependent insulinotropic peptide response while no change in glucagon-like peptide-1 responses was detected.Conclusions: The data presented suggest that casein per se did not modulate the postprandial triglyceride response in type 2 diabetes. When added to carbohydrate, casein suppressed the triglyceride response in the chylomicron-rich fraction, increased insulin and glucagon but did not affect the incretin responses.</description><dc:title>Acute effects of casein on postprandial lipemia and incretin responses in type 2 diabetic subjects</dc:title><dc:creator>L. Brader, L. Holm, L. Mortensen, C. Thomsen, A. Astrup, J.J. Holst, M. de Vrese, J. Schrezenmeir, K. Hermansen</dc:creator><dc:identifier>10.1016/j.numecd.2009.03.019</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-05-28</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-05-28</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>101</prism:startingPage><prism:endingPage>109</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000453/abstract?rss=yes"><title>Obesity and changes in urine albumin/creatinine ratio in patients with type 2 diabetes: The DEMAND Study</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000453/abstract?rss=yes</link><description>Abstract: Background and aims: Obesity is a potential risk factor for renal disease in non-diabetic subjects. It remains unclear whether this also applies to diabetic patients. We investigated whether obesity predicted changes in albumin excretion rate in individuals with type 2 diabetes.Methods and results: Fifty Italian diabetes outpatient clinics enrolled a random sample of 1289 patients. A morning spot urine sample was collected to determine urinary albumin/creatinine ratio (ACR) at baseline and after 1 year from the study initiation. Progression of albumin excretion was defined as a doubling in ACR, while regression was defined as a 50% reduction. Multivariate logistic regression analyses were used to evaluate correlates of these outcomes. Data are expressed as odds ratios (OR) with 95% confidence intervals (CI).The risk of progression increased by 7% (OR=1.07; 95%CI 1.00–1.15) for every 5-cm increase in waist circumference measured at baseline, and by 17% (OR=1.17; 95%CI 1.03–1.33) for every one-unit increase in BMI during follow-up. The likelihood of regression was not independently associated with any of the variables investigated. The effect of obesity on progression of ACR was independent of metabolic control, blood pressure, treatment, and baseline level of albumin excretion.Conclusions: We found a tight link between obesity and changes in albumin excretion in diabetic subjects, suggesting potential benefits of interventions on body weight on end-organ renal damage.</description><dc:title>Obesity and changes in urine albumin/creatinine ratio in patients with type 2 diabetes: The DEMAND Study</dc:title><dc:creator>M.C.E. Rossi, A. Nicolucci, F. Pellegrini, M. Comaschi, A. Ceriello, D. Cucinotta, C. Giorda, B. Pomili, U. Valentini, G. Vespasiani, S. De Cosmo</dc:creator><dc:identifier>10.1016/j.numecd.2009.02.013</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-05-18</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-05-18</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>110</prism:startingPage><prism:endingPage>116</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000660/abstract?rss=yes"><title>Effects of a dairy product (pecorino cheese) naturally rich in cis-9, trans-11 conjugated linoleic acid on lipid, inflammatory and haemorheological variables: A dietary intervention study</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000660/abstract?rss=yes</link><description>Abstract: Background and aim: Some studies recently reported a favourable effect for cis-9, trans-11 conjugated linoleic acid (CLA) on plasma lipoprotein profile of healthy subjects. Aim of this crossover intervention study was to evaluate the influence of a short-term dietary intake of a cheese derived from sheep's milk naturally rich in CLA on several atherosclerotic biomarkers, in comparison with a commercially available cheese.Methods and results: Ten subjects (6 F; 4 M) with a median age of 51.5 followed for 10 weeks a diet containing 200g/week of cheese naturally rich in CLA (intervention period) and for the same period a diet containing a commercially available cheese of the same quantity (placebo period). Consumption of the dairy product naturally rich in cis-9, trans-11 CLA determined a significant (p&lt;0.05) reduction in inflammatory parameters such as interleukin-6 (pre: 8.08±1.57 vs. post: 4.58±0.94pg/mL), interleukin-8 (pre: 45.02±5.82 vs. post: 28.59±2.64pg/mL), and tumour necrosis factor-α (pre: 53.58±25.67 vs. post: 32.09±17.42pg/mL) whereas no significant differences in the placebo period were observed. With regard to haemorheological parameters, the test period significantly ameliorated erythrocytes' filtration rate (pre: 7.61±0.71% vs. post: 9.12±0.97%; p=0.03) with respect to the placebo period. Moreover, a reduction in the extent of platelet aggregation, induced by arachidonic acid [pre: 87.8±1.76% vs. post: 77.7±3.56%; p=0.04] was observed during the test period in comparison with the placebo period.Conclusions: Dietary short-term intake of the tested dairy product naturally rich in cis-9, trans-11 CLA appeared to cause favourable biochemical changes of atherosclerotic markers.</description><dc:title>Effects of a dairy product (pecorino cheese) naturally rich in cis-9, trans-11 conjugated linoleic acid on lipid, inflammatory and haemorheological variables: A dietary intervention study</dc:title><dc:creator>F. Sofi, A. Buccioni, F. Cesari, A.M. Gori, S. Minieri, L. Mannini, A. Casini, G.F. Gensini, R. Abbate, M. Antongiovanni</dc:creator><dc:identifier>10.1016/j.numecd.2009.03.004</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-05-28</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-05-28</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>117</prism:startingPage><prism:endingPage>124</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000581/abstract?rss=yes"><title>Curcumin prevents human aortic smooth muscle cells migration by inhibiting of MMP-9 expression</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000581/abstract?rss=yes</link><description>Abstract: Background and aim: The migration of vascular smooth muscle cells from the tunica media to the subendothelial region is a key event in the development of atherosclerosis. Curcumin, which is consumed daily by millions of people, is a polyphenol derived from the plant Curcuma longa. In this study, we investigated the effects of curcumin on tumor necrosis factor-α (TNF-α)-induced cell migration, the formation of intracellular reactive oxygen species (ROS), the translocation of nuclear factor-κB (NFκB) and the activation and expression of MMP-9 in human aortic smooth muscle cells (HASMCs).Methods and results: The Matrigel migration assay showed that curcumin (10 and 20μmol/l) effectively inhibited TNF-α-induced migration of HASMCs as compared with the control group. To explain this inhibitory effect, MMP-9 was assayed by gelatin zymography and Western blot. The results indicated that curcumin inhibited MMP-9 activity and expression. Furthermore, the production of ROS and the nuclear translocation of NF-κB p50 and p65 induced by TNF-α were dose-dependently suppressed by curcumin pretreatment.Conclusion: These results indicate that curcumin has anti-inflammatory properties and may prevent the migration of HASMCs by suppressing MMP-9 expression through down-regulation of NF-κB.</description><dc:title>Curcumin prevents human aortic smooth muscle cells migration by inhibiting of MMP-9 expression</dc:title><dc:creator>Y.-M. Yu, H.-C. Lin</dc:creator><dc:identifier>10.1016/j.numecd.2009.03.001</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-05-18</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-05-18</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>125</prism:startingPage><prism:endingPage>132</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309000659/abstract?rss=yes"><title>Periodontitis is associated with altered plasma fatty acids and cardiovascular risk markers</title><link>http://www.nmcd-journal.com/article/PIIS0939475309000659/abstract?rss=yes</link><description>Abstract: Background and aims: In periodontitis it has been found that some perturbation exists in lipid biomarkers, such as increased serum total cholesterol and low-density lipoprotein cholesterol. Nevertheless, the relationship between fatty acids and periodontitis has been demonstrated only in a few studies and remains controversial. The aim of this investigation was to explore the effects of periodontitis on a cluster of traditional and novel cardiovascular risk factors such as plasma-lipids profile, types of plasma fatty acids, adhesion molecules and systemic inflammatory markers.Methods and results: At a university dental school, 56 patients all over 35 years old were enrolled and invited to participate in the study. Total plasma fatty acids, saturated, n-6 polyunsaturated and monounsaturated fatty acids, peroxidability index, soluble VCAM, TNF-α, cholesterol, triacylglycerols, and VLDL-c were significantly higher in the periodontitis group compared to the non-periodontitis group.Conclusions: This close association found between plasma triacylglycerols, LDL-c, saturated fatty acids, polyunsaturated fatty acids, total amount of fatty acids and coenzyme Q10 with some periodontal data such as periodontal probing depth, recession of the gingival margin and clinical attachment level (Pearson correlation between 0.3 and 0.6), leads to the conclusion that there is an inter-relationship between periodontitis, plasma fatty acids profile and the increase in metabolic risk factors for cardiovascular diseases.</description><dc:title>Periodontitis is associated with altered plasma fatty acids and cardiovascular risk markers</dc:title><dc:creator>M.C. Ramirez-Tortosa, J.L. Quiles, M. Battino, S. Granados, J.M. Morillo, S. Bompadre, H.N. Newman, P. Bullon</dc:creator><dc:identifier>10.1016/j.numecd.2009.03.003</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-06-08</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-06-08</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>133</prism:startingPage><prism:endingPage>139</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309001896/abstract?rss=yes"><title>Endothelial dysfunction in metabolic syndrome: Prevalence, pathogenesis and management</title><link>http://www.nmcd-journal.com/article/PIIS0939475309001896/abstract?rss=yes</link><description>Abstract: The metabolic syndrome (MetS) is characterized by the presence of central obesity, impaired glucose metabolism, dyslipidemia and hypertension. Several studies showed that MetS is associated with increased risk for type 2 diabetes mellitus (T2DM) and vascular events. All components of MetS have adverse effects on the endothelium. Endothelial dysfunction plays a role in the pathogenesis of atherosclerosis and might also increase the risk for insulin resistance and T2DM. We review the prevalence and pathogenesis of endothelial dysfunction in MetS. We also discuss the potential effects of lifestyle measures and pharmacological interventions on endothelial function in these patients. It remains to be established whether improving endothelial function in MetS will reduce the risk for T2DM and vascular events.</description><dc:title>Endothelial dysfunction in metabolic syndrome: Prevalence, pathogenesis and management</dc:title><dc:creator>K. Tziomalos, V.G. Athyros, A. Karagiannis, D.P. Mikhailidis</dc:creator><dc:identifier>10.1016/j.numecd.2009.08.006</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-10-15</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-10-15</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>140</prism:startingPage><prism:endingPage>146</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309001197/abstract?rss=yes"><title>Food habits and body composition in children and adolescents of Asian Indian origin</title><link>http://www.nmcd-journal.com/article/PIIS0939475309001197/abstract?rss=yes</link><description>Childhood overweight and obesity has become a major public health burden in developing countries (e.g. India) owing to its strong association with risk factors for adult chronic diseases such as type 2 diabetes mellitus, coronary heart disease, etc., and subsequent adverse health outcomes in later life. In the Indian subcontinent, the occurrence of overweight and obesity among children and adolescents is essentially related to their changing lifestyle including changes in food habits concomitant with effective modernization . Food intake is related to obesity not only in terms of the volume of food ingested but also in terms of the composition and quality of the food . The present cross-sectional study was aimed at looking into the association between anthropometric measurements and body composition characteristics with food patterns among children and adolescents in Calcutta, India. A total of 393 healthy children and adolescents (Boys=241 and Girls=152) aged 8–18 years took part in the study. The participants were selected randomly from eight schools in Calcutta, India. Height, weight, circumferences of mid upper arm (MUAC), waist (MWC), hip as well as skinfold thickness were measured. Percentage of body fat, body mass index (BMI) and basal metabolic rate (BMR) were measured using an Omron body fat analyser. A pre-tested open-ended schedule was used to obtain weekly consumption (frequency) of foodstuffs. The mean age of boys and girls was 13.5 years (SD=2.0) and 12.5 years (SD=2.5) respectively. The weekly consumption of processed fast foods, cream rich fast foods, fried snacks, soft drinks, sweets and fats &amp; oils was relatively higher compared to other food items such as leafy vegetables and fish. In fact, 61.8% of participants hadn't consumed leafy vegetables even once in a week. On the other hand 7.6% of participants consumed fried snacks ten times in a week. In our study a significant positive association between fast foods (both fried and cream based) and body composition measures (BMI, MWC, WHR and SF4) was observed as reported in other studies . The reason could be due to the fact that fast foods contain high levels of trans fatty acids (TFA) that contributes to an increase in blood cholesterol levels and reduces the protective high-density cholesterol levels in the blood. In fact, TFA has a higher tendency to promote high levels of low-density lipoprotein like saturated fatty acids. TFA, in Indian diets, are mostly derived from Vanaspati (hydrogenated vegetable oil), a type of cooking medium often used to prepare snacks and sweets . Furthermore, it was also observed that a variety of sweets, snacks, condiments, entrees, and carbohydrates were positively associated with body fatness while vegetable consumption was negatively associated with body fatness. Moreover, the significant positive associations of egg, fried snacks and Bengalee sweets consumption with central obesity measures suggested that these foods might have an adverse effect on central body fat distribution. It is noteworthy to mention that a significant positive association was also evident between atherogenic body fatness (e.g. WHR) and the intake of a variety of fast foods, soft drinks and sweets and this warrants early effective lifestyle intervention.</description><dc:title>Food habits and body composition in children and adolescents of Asian Indian origin</dc:title><dc:creator>A. Ghosh, R. Dutta</dc:creator><dc:identifier>10.1016/j.numecd.2009.04.016</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-08-17</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-08-17</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e1</prism:endingPage></item><item rdf:about="http://www.nmcd-journal.com/article/PIIS0939475309001215/abstract?rss=yes"><title>Addition of different soluble fiber fractions to oven baked products is not always a successful tool for reducing the Glycemic Index</title><link>http://www.nmcd-journal.com/article/PIIS0939475309001215/abstract?rss=yes</link><description>In the 18th issue of “Nutrition Metabolism and Cardiovascular Diseases”, Marangoni and Poli  propose that the addition of a mix of fibers to bread and biscuits markedly reduces the Glycemic Index (GI). Fifteen young healthy non-obese subjects consumed ordinary bread and biscuits enriched with fiber in 75g of available carbohydrate portions. The authors demonstrate a 21% and 41% reduction of GI respectively in bread and biscuits. The fibers used were mainly soluble and the total fiber content was 5–6%. The difficulty in introducing the recommended fiber amount (at least 14g/1000kcal/day) from natural foods, to avoid the frequent gastrointestinal side effects, favored the fiber-fortified foods that are diffuse in Western Countries. Many studies report a significant GI reduction by adding fiber (generally soluble) to bread and oven baked products. Surprisingly, our recent observations on beta-glucan enriched oven baked products (crackers) do not confirm this effect .</description><dc:title>Addition of different soluble fiber fractions to oven baked products is not always a successful tool for reducing the Glycemic Index</dc:title><dc:creator>C. Tubili, L. Morviducci, M.R. Nardone, S. Agrigento, N. Villani</dc:creator><dc:identifier>10.1016/j.numecd.2009.04.019</dc:identifier><dc:source>Nutrition, Metabolism &amp; Cardiovascular Diseases 20, 2 (2010)</dc:source><dc:date>2009-08-19</dc:date><prism:publicationName>Nutrition, Metabolism &amp; Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2009-08-19</prism:publicationDate><prism:volume>20</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0939-4753(10)X0002-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e2</prism:startingPage><prism:endingPage>e3</prism:endingPage></item></rdf:RDF>