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		<title>International Chair on Cardiometabolic Risk News Feed</title>
		<link>http://www.cardiometabolic-risk.org/</link>
		<description></description>
		<language>en</language>
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			<title>International Chair on Cardiometabolic Risk News Feed</title>
			<url>http://www.cardiometabolic-risk.org/</url>
			<link>http://www.cardiometabolic-risk.org/</link>
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		<lastBuildDate>Fri, 30 Jul 2010 08:00:00 -0400</lastBuildDate>
		
		
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			<title>The associations of interleukin-6 (IL-6) and downstream inflammatory markers with risk of cardiovascular disease: the Caerphilly Study. Atherosclerosis 2010;209:551-7 </title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/921/index.html</link>
			<description>Patterson CC, Smith AE, Yarnell JW, Rumley A, Ben-Shlomo Y, Lowe GD.</description>
			<content:encoded><![CDATA[<p>Patterson CC, Smith AE, Yarnell JW, Rumley A, Ben-Shlomo Y, Lowe GD.<br /> <br /> The purpose of this study was to investigate the associations of interleukin (IL)-6 with coronary heart disease (CHD) and ischemic stroke events and to examine whether IL-6 plays a role in mediating the associations of several downstream inflammatory markers with CHD and ischemic stroke. The study cohort was derived from the prospective Caerphilly Study and included 2,208 men aged 45-64 years with a median follow-up of 13.4 years from which 486 men experienced a cardiovascular event. Results showed that circulating levels of the proinflammatory cytokine, IL-6, were significantly associated with risk of CHD. The study confirmed that plasma IL-6 levels were significantly associated with circulating levels of several downstream inflammatory markers such as C-reactive protein (CRP), fibrinogen, plasma viscosity and total and neutrophil leucocyte counts. In multivariate a analysis, the association between IL-6 and CHD and total cardiovascular disease was maintained, while the associations between downstream inflammatory markers and cardiovascular disease were attenuated to non-significance after adjustment for IL-6. These results suggest that IL-6 could be a mediator of the associations observed between several downstream inflammatory markers and CHD risk.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=551[page]+AND+patterson+cc[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Inflammation</category>
			<category>Cardiovascular Disease</category>
			
			
			<pubDate>Fri, 30 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Association of pericardial fat accumulation rather than abdominal obesity with coronary atherosclerotic plaque formation in patients with suspected coronary artery disease. Atherosclerosis 2010;209:573-8</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/922/index.html</link>
			<description>Konishi M, Sugiyama S, Sugamura K, Nozaki T, Ohba K, Matsubara J, Matsuzawa Y, Sumida H, Nagayoshi...</description>
			<content:encoded><![CDATA[<p>Konishi M, Sugiyama S, Sugamura K, Nozaki T, Ohba K, Matsubara J, Matsuzawa Y, Sumida H, Nagayoshi Y, Nakaura T, Awai K, Yamashita Y, Jinnouchi H, Matsui K, Kimura K, Umemura S, Ogawa H.<br /> <br /> The authors in this study wanted to determine the association between pericardial fat volume (PFV) and the presence of early-stage coronary plaques using computed tomography in 171 consecutive patients suspected of coronary artery disease with a mean age of 66±11 years. Results showed that PFV correlated significantly with the presence of any coronary plaques. In fact, through multivariate regression analyses, PFV, but not waist circumference, was significantly and independently associated with the presence of coronary plaques, particularly nonstenotic and noncalcified plaques. Moreover, ROC analysis indicated that PFV could be clinically useful for assessment of coronary plaques detected by multislice CT. These results suggest that pericardial fat deposition may be more strongly associated with coronary atherogenesis than abdominal fat deposition.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed/19892354" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Ectopic Fat</category>
			<category>Cardiovascular Disease</category>
			<category>Abdominal Obesity / Body Fat Distribution</category>
			
			
			<pubDate>Fri, 30 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Nonalcoholic fatty liver disease as the transducer of hepatic oversecretion of very-low-density lipoprotein-apolipoprotein B-100 in obesity. Arterioscler Thromb Vasc Biol 2010;30:1043-50</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/919/index.html</link>
			<description>Chan DC, Watts GF, Gan S, Wong AT, Ooi EM, Barrett PH.</description>
			<content:encoded><![CDATA[<p>Chan DC, Watts GF, Gan S, Wong AT, Ooi EM, Barrett PH.<br /> <br /> This study was conducted to examine the association between intrahepatic fat content and VLDL apolipoprotein (apo) B100 kinetics and the impact of a moderate weight loss on this relationship. Results showed that elevated liver fat content was predictive of VLDL apo B100 oversecretion, and that the reduction of liver fat with weight loss was significantly associated with a corresponding decrease in VLDL apo B100 secretion. It was also found that liver fat content was significantly associated with intra-abdominal (visceral) fat, insulin resistance, dietary fat intake, and the VLDL apo B100 concentrations and secretion rate. However, liver fat content was not associated with plasma concentrations of retinol-binding protein 4, fetuin A, adiponectin, interleukin-6, and tumor necrosis factor-alpha. These kinetic studies of VLDL apo B100 metabolism suggest an important role of liver fat in the dyslipidemia associated with abdominal obesity and the beneficial impact of weight loss observed on liver fat with the corresponding decrease in VLDL apo B100 secretion.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=1043[page]+AND+chan+dc[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Ectopic Fat</category>
			<category>Lipids/Lipoproteins</category>
			<category>Weight Loss</category>
			
			
			<pubDate>Thu, 29 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Relation between visceral fat and coronary artery disease evaluated by multidetector computed tomography. Atherosclerosis 2010;209:481-6</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/920/index.html</link>
			<description>Marques MD, Santos RD, Parga JR, Rocha-Filho JA, Quaglia LA, Miname MH, Avila LF.</description>
			<content:encoded><![CDATA[<p>Marques MD, Santos RD, Parga JR, Rocha-Filho JA, Quaglia LA, Miname MH, Avila LF.<br /> <br /> The purpose of this study was to examine whether computed tomography (CT) adiposity measurements such as intra-abdominal (visceral) adipose tissue, subcutaneous adipose tissue and hepatic fat, are associated with coronary artery disease (CAD) assessed by cardiac CT. Therefore, 125 consecutive subjects (57% men, age 56.0±12 years) referred to CT angiography were evaluated in this study. No association was found between waist and hip circumferences or body mass index with CAD. In a multivariate analysis, only intra-abdominal (visceral) fat (measured at T12-L1) and age were independent predictors of CAD. It was also found that the presence of metabolic syndrome identified by the International Diabetes Federation clinical criteria was associated with the presence of coronary artery calcification. These results support the notion that intra-abdominal fat, assessed by CT, is an independent marker of CAD.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=481[page]+AND+marques+md[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Cardiovascular Disease</category>
			<category>Abdominal Obesity / Body Fat Distribution</category>
			
			
			<pubDate>Thu, 29 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Exercise training versus diet-induced weight-loss on metabolic risk factors and inflammatory markers in obese subjects: a 12-week randomized intervention study. Am J Physiol Endocrinol Metab 2010;298:E824-31</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/917/index.html</link>
			<description>Christiansen T, Paulsen SK, Bruun JM, Pedersen SB, Richelsen B.</description>
			<content:encoded><![CDATA[<p>Christiansen T, Paulsen SK, Bruun JM, Pedersen SB, Richelsen B.<br /> <br /> In this study, the authors sought to investigate independent and combined effects of exercise and weight loss on inflammatory markers in circulation, in adipose tissue and in skeletal muscle of obese subjects. Seventy-nine obese subjects were randomized into a 12-week intervention. The first group was assigned to exercise only (EXO), the second group was prescribed a diet-induced weight loss using a very low energy diet (DIO), and the third group was asked to participate to an exercise and a diet-induced weight loss (DEX) program. The results showed an overall decrease in the circulating proinflammatory markers in response to marked weight loss (11%) in the two diet restriction groups, but there was no additional effect of exercise on the inflammatory profile. Among the emerging inflammatory markers related to obesity, the authors found that macrophage inflammatory protein-1 (MIP-1) and interleukin (IL)-15 were significantly reduced in the DIO and DEX groups, with no effect in the EXO group. In addition, no associations between IL-15 and measures of fat distribution were found. Moreover, they observed no evidence of an exercise-induced anti-inflammatory effect in skeletal muscle tissue. Therefore, the exercise-induced improvements in metabolic complications do not include the inflammatory profile which is in contrast with the beneficial effects of diet-induced weight loss observed in inflammatory markers.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=E824[page]+AND+christiansen[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Inflammation</category>
			<category>Physical Activity/Exercise</category>
			<category>Weight Loss</category>
			
			
			<pubDate>Wed, 28 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>The effects of salsalate on glycemic control in patients with type 2 diabetes: a randomized trial. Ann Intern Med 2010 ;152:346-57</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/918/index.html</link>
			<description>Goldfine AB, Fonseca V, Jablonski KA, Pyle L, Staten MA, Shoelson SE; TINSAL-T2D (Targeting...</description>
			<content:encoded><![CDATA[<p>Goldfine AB, Fonseca V, Jablonski KA, Pyle L, Staten MA, Shoelson SE; TINSAL-T2D (Targeting Inflammation Using Salsalate in Type 2 Diabetes) Study Team.<br /> <br /> Many studies have shown that inflammation is implicated in the pathogenesis of insulin resistance and type 2 diabetes. Consequently, a clinical study was conducted to test an anti-inflammatory drug called salsalate, a nonacetylated prodrug of salicylate that has been shown to decrease blood glucose concentration. The TINSAL-T2D (Targeting Inflammation Using Salsalate in Type 2 Diabetes) trial was designed to evaluate whether this generic and inexpensive drug was safe, tolerated, and efficacious in patients with type 2 diabetes. Results of the study showed that salsalate lowered HbA1c and other measures of glycemic control. In addition, it lowered circulating triglyceride levels and raised adiponectin concentrations. Thus, these results suggest that salsalate has beneficial effects on glucose homeostasis by improving measures of glycemic control over the 3-month trial. Considering the anti-inflammatory nature of this drug, these results support the fact that inflammation is associated with type 2 diabetes. More clinical studies must be conducted to confirm these findings.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=346[page]+AND+goldfine[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Diabetes</category>
			<category>Inflammation</category>
			<category>Clinical Trials</category>
			
			
			<pubDate>Wed, 28 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Influence of leptin, adiponectin, and resistin on the association between abdominal adiposity and arterial stiffness. Am J Hypertens 2010;23:501-7</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/915/index.html</link>
			<description>Windham BG, Griswold ME, Farasat SM, Ling SM, Carlson O, Egan JM, Ferrucci L, Najjar SS.</description>
			<content:encoded><![CDATA[<p>Windham BG, Griswold ME, Farasat SM, Ling SM, Carlson O, Egan JM, Ferrucci L, Najjar SS.<br /> <br /> This study was conducted to examine the independent contributions of adipokines such as leptin, adiponectin and resistin, to the relationship between abdominal adiposity and arterial stiffness measured by pulse wave velocity. The study cohort included 749 participants from the Baltimore Longitudinal Study of Aging. This cross-sectional analysis reported that the association between abdominal adiposity and arterial stiffness was independent of well-known potential confounders but was eliminated when leptin was included in the analysis. In contrast, neither adiponectin nor resistin significantly altered the relationship between arterial stiffness and adiposity even though adiponectin, resistin as well as leptin were independently associated with arterial stiffness. Moreover, the associations between adipokines and arterial stiffness were not affected by adiposity. Thus, these results support the contribution of adipokines to vascular complications associated with obesity such as arterial stiffness.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=501[page]+AND+windham+bg[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Adipokines</category>
			<category>Cardiovascular Disease</category>
			<category>Abdominal Obesity / Body Fat Distribution</category>
			
			
			<pubDate>Tue, 27 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Effects of incretin hormones on beta-cell mass and function, body weight, and hepatic and myocardial function. Am J Med 2010;123:S19-27</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/916/index.html</link>
			<description>Mudaliar S, Henry RR.</description>
			<content:encoded><![CDATA[<p> Mudaliar S, Henry RR.<br> <br> The endogenous incretin hormones, glucagonlike peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are released from the gastrointestinal tract after nutrient stimulation and play a major role in glucose homeostasis. Thus, incretin hormones represent a novel therapeutic target for the treatment of diabetes. In clinical studies, both exenatide and liraglutide (GLP-1 receptor agonists which are resistant to DPP-4 degradation) are known to improve <span style="font-size: 9pt; color: black; font-family: Symbol">b</span>-cell function and glycemia with minimal hypoglycemia. This review aimed to examine the extraglycemic effects of the incretins and to justify the therapeutic rationale for incretin-based strategies in patients with type 2 diabetes. First of all, therapeutic agents like incretins have been shown to inhibit <span style="font-size: 10pt; color: black; font-family: Symbol"><span style="font-size: 9pt; color: black; font-family: Symbol">b</span></span>-cell apoptosis and increase islet proliferation/replication. Moreover, the use of these agents was also reported to be associated with reduced body weight, and in some studies, had favourable effects on blood pressure, diabetic dyslipidemia, myocardial contractility, hepatic and endothelial function. These effects have the potential to provide a better control of glucose homeostasis and also decrease multiple cardiovascular risk factors that are observed in patients with diabetes.<br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=S19[page]+AND+Mudaliar+S[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a>  </p>]]></content:encoded>
			<category>News</category>
			<category>Diabetes</category>
			<category>Cardiovascular Disease</category>
			<category>Obesity</category>
			
			
			<pubDate>Tue, 27 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Effects of coffee consumption on subclinical inflammation and other risk factors for type 2 diabetes: a clinical trial. Am J Clin Nutr 2010;91:950-7</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/913/index.html</link>
			<description>Kempf K, Herder C, Erlund I, Kolb H, Martin S, Carstensen M, Koenig W, Sundvall J, Bidel S, Kuha S,...</description>
			<content:encoded><![CDATA[<p> Kempf K, Herder C, Erlund I, Kolb H, Martin S, Carstensen M, Koenig W, Sundvall J, Bidel S, Kuha S, Jaakko T.<br> <br> This study was conducted to examine the effects of daily coffee consumption on biomarkers of coffee intake, subclinical inflammation, oxidative stress, glucose and lipid metabolism. The cohort included 47 chronic coffee drinkers who abstained for one month from coffee drinking, thereafter they consumed 4 cups/day of filtered coffee in the second month and finally 8 cups/day of filtered coffee for the last month. Results showed that coffee consumption generated an increase in coffee-derived compounds, particularly serum caffeine, chlorogenic acid, and caffeic acid metabolites. Changes in some markers of inflammation and oxidative stress were also observed, and suggested an anti-inflammatory effect of coffee drinking. There was a significant decrease in circulating interleukin (IL)-18 concentrations and serum 8-isoprostane levels, but no changes in systemic C-reactive protein or IL-6 concentrations. They also observed a significant increase in adiponectin concentrations with coffee consumption. Moreover, beneficial effects on the lipid profile such as increases in HDL cholesterol, and apolipoprotein AI as well as decreases in LDL cholesterol/HDL cholesterol and apolipoprotein B/apolipoprotein AI ratios were observed. However, no effect of coffee consumption was reported on glucose metabolism. Thus, these findings suggest a positive impact of coffee consumption on some cardiometabolic risk markers.<br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=950[page]+AND+kempf[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a>  </p>]]></content:encoded>
			<category>News</category>
			<category>Diabetes</category>
			<category>Inflammation</category>
			<category>Nutrition</category>
			
			
			<pubDate>Mon, 26 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Adipose tissue-specific regulation of angiotensinogen in obese humans and mice: impact of nutritional status and adipocyte hypertrophy. Am J Hypertens 2010;23:425-31</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/914/index.html</link>
			<description>Yasue S, Masuzaki H, Okada S, Ishii T, Kozuka C, Tanaka T, Fujikura J, Ebihara K, Hosoda K,...</description>
			<content:encoded><![CDATA[<p> Yasue S, Masuzaki H, Okada S, Ishii T, Kozuka C, Tanaka T, Fujikura J, Ebihara K, Hosoda K, Katsurada A, Ohashi N, Urushihara M, Kobori H, Morimoto N, Kawazoe T, Naitoh M, Okada M, Sakaue H, Suzuki S, Nakao K.<br> <br> The aims of this study were to investigate the association between the level of expression of adipose tissue-derived angiotensinogen secretion (A-AGT-S) and indices of body fat mass, to examine the regulation of A-AGT-S in relation to obesity in humans, and finally to assess the contribution of A-AGT-S to plasma AGT in mouse models of obesity and weight reduction. The amount of A-AGT-S was estimated by multiplying the mRNA level of AGT/g adipose tissue by body fat mass. The human sample included 46 Japanese subjects who were recruited for subcutaneous abdominal adipose tissue biopsies. The authors found that the secretion of adipose tissue-derived AGT was substantially increased in both obese humans and obese mice and it was correlated with plasma AGT levels in mouse models of obesity and weight reduction. For instance, plasma AGT levels were increased by ­~20% in the obese mouse, whereas they were decreased by ~12% in mice with weight reduction. Moreover, the AGT mRNA levels in adipose tissue were decreased in both obese humans and mice and increased in mice after weight loss, whereas A-AGT-S showed the opposite trend. The authors explained these results in part by triglyceride accumulation and adipocyte hypertrophy in obese adipose tissue. Thus, these results suggest that adipose tissue-derived AGT could contribute to circulating AGT levels and consequently play a role in obesity-related metabolic diseases.<br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=425[page]+AND+yasue+s[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a>  </p>]]></content:encoded>
			<category>News</category>
			<category>Adipose Tissue</category>
			<category>Hypertension </category>
			<category>Obesity</category>
			
			
			<pubDate>Mon, 26 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Prevalence of the metabolic syndrome as influenced by the measure of obesity employed. Am J Cardiol 2010;105:1306-12</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/911/index.html</link>
			<description>Vega GL, Barlow CE, Grundy SM. </description>
			<content:encoded><![CDATA[<p>Vega GL, Barlow CE, Grundy SM.<br /> <br /> The objectives of the present study were to test whether the measurement of waist girth is better compared to other measurements of obesity to quantify the prevalence of the metabolic syndrome and to examine if obesity should be included among the diagnostic criteria. A cohort of 8,879 women and 23,145 men in the Cooper Center Longitudinal Study was used for this analysis. Percentage body fat, body mass index, and truncal subcutaneous fat were strongly correlated with waist girth and were comparable in identifying the metabolic syndrome prevalence with the National Cholesterol Education Program-Adult Treatment Panel III clinical criteria. Removing obesity measures from the diagnostic criteria of metabolic syndrome identified a smaller group of patients who were at higher risk for cardiovascular disease. Therefore, identification of patients with metabolic syndrome is useful but heterogeneous in its presentation which should influence short-term and long-term clinical outcomes.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=1306[page]+AND+Vega+GL[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Metabolic Syndrome</category>
			<category>Obesity</category>
			
			
			<pubDate>Fri, 23 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Low-fat dietary pattern and lipoprotein risk factors: the Women's Health Initiative Dietary Modification Trial. Am J Clin Nutr 2010;91:860-74</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/912/index.html</link>
			<description>Howard BV, Curb JD, Eaton CB, Kooperberg C, Ockene J, Kostis JB, Pettinger M, Rajkovic A, Robinson...</description>
			<content:encoded><![CDATA[<p> Howard BV, Curb JD, Eaton CB, Kooperberg C, Ockene J, Kostis JB, Pettinger M, Rajkovic A, Robinson JG, Rossouw J, Sarto G, Shikany JM, Van Horn L.<br> <br> The purpose of this article was to investigate the effects of dietary carbohydrate changes on lipids and lipoprotein composition. The data were obtained from the Women’s Health Initiative Dietary Modification Trial, an intervention designed to reduce total fat intake to 20% of energy and to increase vegetable and fruit intake to &#8805;5 servings/day as well as grain intake to &#8805;6 servings/day. The cohort included postmenopausal women who were randomly assigned to an intervention or a comparison group for a mean of 8.1 years. Analyses in a specific sample of postmenauposal women without severe hypertriglyceridemia at baseline revealed no clinically meaningful increases in triglycerides or decreases in HDL cholesterol associated with the increase in complex carbohydrate intake. However, diabetes status and race appeared to have a significant impact on the percentage of change in triglyceride levels between the intervention and control groups. The increase in triglycerides was more marked in diabetic white women with an average increase of 33.8 mg/dl (0.38 mmol/l) compared to 6.4 mg/dl (0.07 mmol/l) in black women with diabetes. Thus, these findings are in contrast with the prior literature since the intervention did not result in clinically meaningful increases in triglycerides or decreases in HDL cholesterol in the majority of women. </p>
<p> In his comment, Willet WC <a href="http://www.ncbi.nlm.nih.gov/pubmed/20181816" target="_blank" class="undefined" >(Am J Clin Nutr 2010;91:829-30)</a> qualified the findings of this study as remarkable considering the large literature that shows an increase in plasma fasting triglycerides and reduction of HDL cholesterol concentrations when replacing dietary fat with carbohydrates. However, he criticized the lack of compelling reasons to explain their findings and he proposed that it is probably the large increase in fruits and vegetables, whole grains and protein that counterbalanced the adverse effects of fat reduction. However, he suggested that the more plausible explanation is an overreporting of compliance with fat reduction by the women in the intervention group.<br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=860[page]+AND+howard+b[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Nutrition</category>
			<category>Lipids/Lipoproteins</category>
			
			
			<pubDate>Fri, 23 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Prevalence of diabetes among men and women in China. N Engl J Med 2010;362:1090-101</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/909/index.html</link>
			<description>Yang W, Lu J, Weng J, Jia W, Ji L, Xiao J, Shan Z, Liu J, Tian H, Ji Q, Zhu D, Ge J, Lin L, Chen L,...</description>
			<content:encoded><![CDATA[<p>Yang W, Lu J, Weng J, Jia W, Ji L, Xiao J, Shan Z, Liu J, Tian H, Ji Q, Zhu D, Ge J, Lin L, Chen L, Guo X, Zhao Z, Li Q, Zhou Z, Shan G, He J; China National Diabetes and Metabolic Disorders Study Group.<br /> <br /> This cross-sectional study was designed to estimate the prevalence of diabetes among Chinese adults. The cohort was composed of a nationally representative sample of 46,239 adults, 20 years of age or older. Results revealed that diabetes has reached epidemic proportions in the general adult population in China. Overall, 92.4 million adults have diabetes which represents 9.7% of the adult population, and in 60.7% of these cases, the diabetes was undiagnosed. Moreover, 148.2 million adults (15.5%) have prediabetes. The prevalence of diabetes increased as a function of age and body weight. In addition, the prevalence of diabetes was higher among urban residents than among rural residents which appeared to be explained in part by the level of economic development and associated lifestyle and diet. Thus, these results suggest that diabetes has become a major public health challenge in China highlighting the importance of national strategies to increase prevention and treatment of diabetes.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed/20335585" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Diabetes</category>
			<category>Epidemiology</category>
			
			
			<pubDate>Thu, 22 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Aerobic exercise training reduces hepatic and visceral lipids in obese individuals without weight loss. Hepatology 2009;50:1105-12</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/910/index.html</link>
			<description>Johnson NA, Sachinwalla T, Walton DW, Smith K, Armstrong A, Thompson MW, George J.</description>
			<content:encoded><![CDATA[<p>Johnson NA, Sachinwalla T, Walton DW, Smith K, Armstrong A, Thompson MW, George J.<br /> <br /> This randomized placebo-controlled study examined whether aerobic exercise training influenced blood, intramyocellular, abdominal and hepatic lipids in 19 sedentary obese men and women. After the four-week intervention program, cardiorespiratory fitness was significantly improved in the exercise group compared to placebo while body weight and body mass index did not change. However, intra-abdominal (visceral) adipose tissue area and volume were reduced in subjects who exercised vs. placebo. Moreover, hepatic triglyceride concentration and plasma free fatty acid levels were also reduced with exercise as compared to placebo. No significant changes were observed in subcutaneous adipose tissue, vastus lateralis intramyocellular triglyceride concentration, proton magnetic resonance spectroscopy-measured hepatic lipid saturation and insulin resistance (HOMA). Results of this study indicate that aerobic exercise training can reduce hepatic lipids and mobilize intra-abdominal adipose tissue without any change in body weight in sedentary obese individuals.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hepatology+%28Baltimore%2C+Md.%29%22%5BJour%5D+AND+1105%5Bpage%5D+AND+2009%5Bpdat%5D&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Physical Activity/Exercise</category>
			<category>Ectopic Fat</category>
			
			
			<pubDate>Thu, 22 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Metabolic syndrome is associated with more pronounced impairment of left ventricle geometry and function in patients with calcific aortic stenosis: a substudy of the ASTRONOMER (Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin). J Am Coll Cardiol 2010;55:1867-74</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/907/index.html</link>
			<description>Pagé A, Dumesnil JG, Clavel MA, Chan KL, Teo KK, Tam JW, Mathieu P, Després JP, Pibarot P;...</description>
			<content:encoded><![CDATA[<p>Pagé A, Dumesnil JG, Clavel MA, Chan KL, Teo KK, Tam JW, Mathieu P, Després JP, Pibarot P; ASTRONOMER Investigators.<br /> <br /> This study was conducted to examine the relationships between metabolic syndrome and the pattern of left ventricular hypertrophy as well as the degree of left ventricular diastolic and systolic dysfunction in patients with asymptomatic aortic stenosis. For that purpose, baseline data of 272 patients from the ASTRONOMER (Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin) study were analyzed. The results revealed that metabolic syndrome was independently associated with a markedly higher prevalence of left ventricular concentric hypertrophy and with impaired myocardial diastolic and systolic functions in patients with calcific aortic stenosis. Therefore, it is suggested that the metabolic alterations linked to intra-abdominal (visceral) obesity and insulin resistance may be important determinants of left ventricular remodelling and function in patients with aortic stenosis.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=1867[page]+AND+Page+A[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Metabolic Syndrome</category>
			<category>Cardiovascular Disease</category>
			
			
			<pubDate>Wed, 21 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Carotid intima-media thickness and presence or absence of plaque improves prediction of coronary heart disease risk: the ARIC (Atherosclerosis Risk In Communities) study. J Am Coll Cardiol 2010;55:1600-7</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/908/index.html</link>
			<description>Nambi V, Chambless L, Folsom AR, He M, Hu Y, Mosley T, Volcik K, Boerwinkle E, Ballantyne CM.</description>
			<content:encoded><![CDATA[<p> Nambi V, Chambless L, Folsom AR, He M, Hu Y, Mosley T, Volcik K, Boerwinkle E, Ballantyne CM.<br> <br> The purpose of this study was to investigate whether carotid intima-media thickness (CIMT) and information about the presence or absence of plaque could improve coronary heart disease (CHD) risk prediction in the ARIC (Atherosclerosis Risk In Communities) study. The study sample for this analysis included 13,145 patients between 45 and 64 years of age. Results showed that using CIMT and plaque information can improve CHD risk prediction. Moreover, adding CIMT and plaque information to traditional risk factors resulted in the reclassification of ­~23% of the subjects, with a net reclassification improvement of 9.9%. However, most of the subjects were reclassified to a lower risk group than to a higher risk group. Indeed, almost 61.9% of those reclassified from the intermediate risk group (5% to 20% estimated 10-year CHD risk) were reclassified to lower risk. Furthermore, plaque presence seemed to have a more profound effect on improving risk prediction in women than in men. Thus, CIMT and identification of plaque presence improves CHD risk prediction in the ARIC study.  </p>
<p> In their comment, Stein JH and Johnson HM <a href="http://www.ncbi.nlm.nih.gov/pubmed/20378079" target="_blank" class="undefined" >(J Am Coll Cardiol 2010;55:1608-10)</a> recognized that this study provided the best evidence to date that CIMT can improve CHD risk prediction. They also underlined the clear conclusions reached regarding CIMT imaging and the fact that these findings validated the recent consensus statement recommendations of combining CIMT and carotid plaque for optimal risk prediction in a specific category of patients.<br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=1600[page]+AND+Nambi[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article </a> </p>]]></content:encoded>
			<category>News</category>
			<category>Cardiovascular Disease</category>
			
			
			<pubDate>Wed, 21 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Physical activity and weight gain prevention. JAMA 2010;303:1173-9</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/905/index.html</link>
			<description>Lee IM, Djoussé L, Sesso HD, Wang L, Buring JE.</description>
			<content:encoded><![CDATA[<p> Lee IM, Djoussé L, Sesso HD, Wang L, Buring JE.<br> <br> The objective of this study was to examine weight changes associated with different physical activity levels in a large cohort of women who were followed for 13 years. This study sample including 34,079 women (mean age: 54.2 years) derived from the Women’s Health Study. This study reported an overall weight gain over time. In a stratified analysis, results showed that in comparison with women who engaged in the equivalent of 420 minutes per week of moderate-intensity physical activity, the two other groups that performed either 150-420 minutes per week or &lt;150 minutes per week gained significantly more weight. Moreover, there was no difference in weight gain between the two less active groups. In addition, the authors observed that the association between physical activity and weight gain was different according to levels of body mass index. For instance, physical activity was inversely related to weight gain only among normal weight women whereas no relation was observed among heavier women. These results suggest that 60 minutes per day of moderate-intensity physical activity is needed to maintain normal weight and prevent weight gain without caloric restriction, but this association is only observed among normal-weight women. On the other hand, these results suggest that heavier women require controlling their caloric intake for weight maintenance.<br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed/20332403" target="_blank" class="undefined" >Pubmed article</a>  </p>]]></content:encoded>
			<category>News</category>
			<category>Physical Activity/Exercise</category>
			<category>Obesity</category>
			<category>Weight Loss</category>
			
			
			<pubDate>Tue, 20 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Caloric sweetener consumption and dyslipidemia among US adults. JAMA 2010;303:1490-7</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/906/index.html</link>
			<description>Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB.</description>
			<content:encoded><![CDATA[<p>Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB.<br /> <br /> The aim of this study was to examine the correlation between consumption of added sugars and lipid variables among US adults. The study cohort included 6,113 adult participants (3,088 women, 3,025 men) of the National Health and Nutrition Examination Survey (NHANES) 1999-2006. The results indicated that an increased consumption of added sugars was associated with alterations in important cardiovascular disease risk factors such as lower HDL cholesterol levels, higher triglyceride levels, and a higher triglycerides/HDL cholesterol ratio. The authors suggest that the dysmetabolic effects of carbohydrates could be largely mediated by fructose which has been shown to increase de novo lipogenesis in the liver, hepatic triglyceride synthesis, and secretion of VLDL. These data support the importance of reducing the consumption of added sugar.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=1490[page]+AND+Welsh+JA[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Lipids/Lipoproteins</category>
			<category>Nutrition</category>
			
			
			<pubDate>Tue, 20 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Macrophage adiponectin expression improves insulin sensitivity and protects against inflammation and atherosclerosis. Diabetes 2010;59:791-9</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/903/index.html</link>
			<description>Luo N, Liu J, Chung BH, Yang Q, Klein RL, Garvey WT, Fu Y.</description>
			<content:encoded><![CDATA[<p>Luo N, Liu J, Chung BH, Yang Q, Klein RL, Garvey WT, Fu Y.<br /> <br /> This interesting study using a unique mouse model was conducted to investigate adiponectin-mediated changes in metabolism in vivo. For that purpose, transgenic mice were developed to specifically express the gene coding for human adiponectin in mouse macrophages. The results showed that macrophage-produced adiponectin induced favourable changes in multiple metabolic pathways in adipose and skeletal muscle tissues resulting in enhanced whole-body glucose tolerance and insulin sensitivity with reduced proinflammatory cytokines. Moreover, the adiponectin expression was associated with reduced whole-body weight and fat mass as well as decrease cholesterol and triglyceride accumulation in the macrophages. In addition, it was also reported that macrophage foam cell formation in atherosclerotic lesions was significantly reduced in transgenic mice crossed with an LDL receptor-deficient mouse model. These observations suggest that adiponectin has important roles in several metabolic pathways with antidiabetic, anti-inflammatory and antiatherogenic functions. This study presents a new and innovative way to investigate the in vivo functions of adiponectin.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=791[page]+AND+Luo+N[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Adipokines</category>
			<category>Metabolism: Animal Studies</category>
			<category>Inflammation</category>
			
			
			<pubDate>Mon, 19 Jul 2010 08:00:00 -0400</pubDate>
			
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			<title>Visceral Adiposity Index: a reliable indicator of visceral fat function associated with cardiometabolic risk. Diabetes Care 2010;33:920-2</title>
			<link>http://www.cardiometabolic-risk.org/news-date/news-item/comm/904/index.html</link>
			<description>Amato MC, Giordano C, Galia M, Criscimanna A, Vitabile S, Midiri M, Galluzzo A; AlkaMeSy Study...</description>
			<content:encoded><![CDATA[<p>Amato MC, Giordano C, Galia M, Criscimanna A, Vitabile S, Midiri M, Galluzzo A; AlkaMeSy Study Group.<br /> <br /> The aim of this study was to elaborate a new sex-specific index to estimate the visceral adiposity dysfunction associated with cardiometabolic risk. The visceral adiposity index (VAI) was based on waist circumference, body mass index, triglycerides and HDL cholesterol levels. It was also modeled on 315 nonobese healthy subjects and validated in 1,498 primary care patients using two multiple logistic regression models to explore possible determinants of cardiovascular and cerebrovascular events. VAI was significantly correlated to metabolic syndrome clinical variables. VAI was independently associated to cardiovascular events, along with age at the time of event, smoking and male sex. Moreover, VAI and age at the time of event were the only independent risk factors for cerebrovascular events. VAI was also inversely associated with insulin sensitivity. These results suggest that VAI might be a useful tool to evaluate the cardiometabolic risk associated with intra-abdominal (visceral) obesity.<br /> <br /> <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=920[page]+AND+amato[author]&amp;cmd=detailssearch" target="_blank" class="undefined" >Pubmed article</a> </p>]]></content:encoded>
			<category>News</category>
			<category>Abdominal Obesity / Body Fat Distribution</category>
			<category>Cardiometabolic Risk</category>
			<category>Metabolic Syndrome</category>
			
			
			<pubDate>Mon, 19 Jul 2010 08:00:00 -0400</pubDate>
			
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