The higher CRP concentrations found in women appear to be due to their greater accumulation of subcutaneous fat than that observed in men.
Aims/hypothesis We previously reported that the plasma levels of the endocannabinoid, 2-arachidonoylglycerol (2-AG), in a cohort of viscerally obese men are directly correlated with visceral adipose tissue (VAT) accumulation and metabolic risk factors including low HDL-cholesterol and high triacylglycerol. It is not known, however, if such correlations persist after vigorous lifestyle interventions that reduce metabolic risk factors. We analysed the changes in endocannabinoid levels in a subsample from the same cohort following a 1 year lifestyle modification programme, and correlated them with changes in VAT and metabolic risk factors. Methods Forty-nine viscerally obese men (average age 49 years, BMI 30.9 kg/m 2 , waist 107.3 cm) underwent a 1 year lifestyle modification programme including healthy eating and physical activity. Plasma levels of 2-AG and the other most studied endocannabinoid, anandamide, were measured by liquid chromatography-mass spectrometry. Anthropometric and metabolic risk factors, including VAT, insulin resistance and glucose intolerance, HDL-cholesterol and triacylglycerol, were measured. Results Most risk factors were improved by the intervention, which led to a significant decrease in body weight (−6.4 kg, p<0.0001), waist circumference (−8.0 cm, p<0.0001) and VAT (−30%, p<0.0001), and in plasma 2-AG (−62.3%, p<0.0001) and anandamide (−7.1%, p=0.005) levels. The decrease in levels of 2-AG but not those of anandamide correlated with decreases in VAT and triacylglycerol levels, and with the increase in HDL 3 -cholesterol levels. Multivariate analyses suggested that decreases in 2-AG and VAT were both independently associated with decreases in triacylglycerol.Conclusions/interpretation This study shows that a strong correlation exists between 2-AG levels and high plasma triacylglycerol and low HDL 3 -cholesterol in viscerally obese men.
Objective-To investigate the effect of exercise training on markers of the lipoprotein-lipid profile and inflammatory markers in postmenopausal overweight/obese women with a moderately elevated systolic blood pressure.Methods-A total of 267 women [mean body mass index (BMI) =32.0±5.7 kg/m 2 and mean age=57.3±6.6 years] underwent a 6-month exercise intervention program. Exercise training was performed 3 to 4 times per week at a targeted heart rate corresponding to 50% of the maximal oxygen consumption.Results-Compared to baseline values, mean change in relative VO 2 max (the primary endpoint) was of 1.18±2.25 mL/min*kg (p<0.0001), mean weight loss was of 1.4±3.3 kg (p<0.0001), mean reduction in waist circumference was of 2.4±6.9 cm (p<0.0001) and systolic blood pressure did not change significantly (−1.2±13.0 mmHg, NS). No changes were observed in markers of the lipoprotein-lipid profile. No changes were observed for plasma levels of C-reactive protein, interleukin-6, tumor necrosis factor-α and adiponectin. Changes in VO 2 max were negatively associated with changes in body weight (r=−0.26, p<0.0001) and waist circumference (r=−0.16, p=0.01), but not with changes in cardiometabolic risk markers. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptAtherosclerosis. Author manuscript; available in PMC 2010 December 1. Conclusion-Although exercise training significantly increased cardiorespiratory fitness in these sedentary, but metabolically healthy obese/overweight women with a moderately elevated systolic blood pressure, no significant improvements were observed in their cardiometabolic risk profile.
Because IL-6 appeared to be clearly associated with visceral adiposity, TNF-alpha rather showed associations with indices of total body fatness. Thus, TNF-alpha may contribute to the insulin resistance of overall obesity, whereas IL-6 may be one of the mediators of the hyperinsulinemic state specifically related to excess visceral adiposity.
Objective-In patients with severe aortic stenosis (AS), we examine the association between: (1) the content of oxidized LDL (oxLDL) in the aortic valve and the degree of inflammation and remodeling; (2) The proportion of small dense LDL particles in the plasma and the presence of oxLDL in the valve along with hemodynamic progression of valve stenosis. Methods and Results-We have examined 102 explanted AS valves. Tissue remodeling, inflammation, and accumulation of oxLDL were determined. A complete plasma lipid profile including the measurement of the relative proportion of small low-density lipoprotein (%LDL Ͻ255Å ) was obtained. Valves with higher oxLDL content had a significantly higher density of inflammatory cells, expression of tumor necrosis factor (TNF)-␣, and increased tissue remodeling score. The %LDL Ͻ255Å was significantly associated with oxLDL score within the aortic valve. In a subset of 59 patients in whom stenosis progression was measured, the %LDL Ͻ255Å correlated with the annualized peak gradient (rϭ0.29; Pϭ0.04). Conclusion-Increased proportion of circulating small dense LDL particles is associated with faster progression rate of stenosis and greater accumulation of oxLDL in the aortic valve. These findings suggest that therapeutic interventions aimed at lowering the production of small dense LDL particles in patients with AS might represent a potentially interesting therapeutic avenue.
The present study is the first to report that MS is associated with a faster disease progression and worse outcome in patients with AS. Such findings open new avenues of research and provide a strong impetus for the elaboration of additional prospective studies focusing on this association.
Cardiovascular disease (CVD) is a leading cause of morbidity and death in many countries worldwide. With the help of epidemiological, metabolic and clinical studies conducted over the past decades, the key factors contributing to the development of CVD have been identified. In this regard, several modifiable (hypertension, smoking, elevated cholesterol or lowdensity lipoprotein-cholesterol concentrations, reduced levels of highdensity lipoprotein-cholesterol, type 2 diabetes) and nonmodifiable (age, sex, genetic predisposition) CVD risk factors have been recognized. Although better acute care and chronic pharmacological management have contributed to reduce CVD mortality, CVD morbidity remains very high. It has been proposed that this situation could be the consequence of the evolving landscape of CVD risk factors, which include, among others, poor nutritional habits and a reduction in physical activity contributing to the epidemic of obesity sweeping the world. However, obesity is heterogeneous both in terms of its etiology and its metabolic complications. Body fat distribution, especially visceral adipose tissue accumulation, has been found to be a major correlate of a cluster of diabetogenic and atherogenic abnormalities that has been described as the metabolic syndrome. The importance of abdominal obesity in association with the development of CVD and type 2 diabetes has been recognized in several studies, beyond the contribution of overall obesity. Additional evidence also suggests that the CVD risk related to the hyperglycemic state observed in subjects with the metabolic syndrome or type 2 diabetes is largely explained by the high prevalence of the metabolic complications of abdominal obesity. Although the presence of the metabolic syndrome clearly increases CVD risk, its clinical diagnosis is not sufficient to classify a patient at high risk for a cardiovascular event because attention must also be paid to the presence of traditional risk factors in the calculation of global CVD risk. The additional information provided by the metabolic syndrome to the risk attributed to traditional risk factors in the calculation of global CVD risk has been defined as global cardiometabolic risk. The fight against abdominal obesity as a major cause of CVD morbidity and mortality will require major societal changes and the involvement of dieticians, kinesiologists and behaviour modification specialists in clinical practice to reshape our physical activity and dietary habits. Finally, the early prevention of overweight/obesity/abdominal obesity in children, starting as early as conception, and the identification of key drivers of unhealthy nutritional and sedentary behaviours are the cornerstone of a successful comprehensive plan to fight CVD morbidity. Les maladies cardiovasculaires (MCV) représentent toujours la première cause de morbidité et mortalité dans plusieurs pays. Les nombreuses études épidémiologiques, métaboliques et cliniques réalisées au cours des dernières années ont permis l'identification des principaux ...
Increased level of circulating ox-LDL is associated with worse fibrocalcific remodelling of valvular tissue in AS. It remains to be determined whether circulating ox-LDL is a risk marker for a highly atherogenic profile and/or a circulating molecule which is actively involved in the pathogenesis of calcific aortic valve disease.
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