1,721,075 research outputs found
Muscle lipid metabolism in the metabolic syndrome
No full textPURPOSE OF REVIEW: The metabolic syndrome has been emphasized as affecting an important subset of individuals at high risk for cardiovascular disease leading the National Cholesterol Educational Program Adult Treatment Panel III in highlighting awareness of insulin-resistance syndrome. Insulin resistance is thought to be an underlying feature of the metabolic syndrome and in the last few years efforts have been performed to assess the effects of ectopic fat accumulation on whole-body glucose metabolism and on the pathogenesis of insulin resistance. RECENT FINDINGS: Abnormality of fatty acid metabolism and ectopic fat accumulation within skeletal muscle has been measured using the traditional biopsy technique but this field of investigation has been exploited considerably more recently thanks to the use of non-invasive H-magnetic resonance spectroscopy. Initial data supported the hypothesis that a strong causal relationship between increased intra-myocellular lipid (IMCL) content and whole-body insulin resistance might exist. Indeed, experimental evidence is still controversial especially when the modulation of the IMCL content is induced by physical exercise and nutritional interventions. SUMMARY: It has been suggested recently that the flux of muscular fatty acids as a source of oxidative energy may play a pivotal role into the development of the abnormalities of muscle and whole-body energy metabolism, potentially as the basis of the pathogenesis of obesity, the metabolic syndrome and type 2 diabetes
The role of non alcoholic fatty liver disease in cardiovascular disease
No full textBackground/Aims: Fatty liver is the hepatic component of the metabolic syndrome. Insulin resistance, the pathogenic driver of the metabolic syndrome, refers to a constellation of features such as overweight/obesity, glucose intolerance, dyslipidemia and hypertension, all of which are important risk factors for cardiovascular disease (CVD). The aim of this article is to summarize the available data linking non-alcoholic fatty liver disease (NAFLD) with CVD. Methods: Two approaches were used to address this issue. First, data in support of the presence of the typical in vivo pathogenic features of atherosclerosis in individuals with NAFLD were described to confirm whether or not the association between NAFLD and CVD is plausible. Second, epidemiological data linking NAFLD with CVD outcome was reviewed. Results: Individuals with NAFLD are characterized by abnormal endothelial function. Data about the carotid intima-media thickness, which as a surrogate marker of atherosclerosis, are controversial, as is higher CAD even if altered myocardial perfusion has been described. Data in support of altered cardiac intermediary metabolism and energy metabolism are more robust. Low-grade inflammation is typically linked to NAFLD and animal studies, suggested that NAFLD may represent a potential mediator of the systemic inflammation. Epidemiologic studies support a causal link between fatty liver and type 2 diabetes but the causal association between NAFLD and CVD is rather weak. Conclusion: NAFLD is characterized by the early onset of the typical metabolic and vascular pathogenic alterations of atherosclerosis. In spite of this background, the evidence for the association between NAFLD and CVD is weak
Ageing and cardiac function. Is there a role of physical exercise?
No full textAgeing of the human heart is characterized bymorphological, functional and metabolic changes regardless the development of ischemic heart disease. Physical exercise is in general considered capable to counteract the onset of these changes; nevertheless short-term interventions and cross sectional studies in older individuals questioned the possibility that physical exercise may revert these alterations. Metabolic factors, development of overt cardiac diseases and probably the timing of the intervention with physical exercise during the life-span of a single individual may explain the controversial results reported in the literature
Is a nutritional therapeutic approach unsuitable for metabolically healthy but obese women?
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Exploring the in vivo mechanisms of action of glucokinase activators in type 2 diabetes
No full textComment on J Clin Endocrinol Metab. 2010 Nov;95(11):5028-36
Letter by Fragasso et al regarding article by Tuunanen et al, Free fatty acid depletion acutely decreases cardiac work and efficiency in cardiomyopathic heart failure
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