Lifestyle modification and endothelial function in obese subjects.
The metabolic syndrome is a cluster of metabolic and vascular abnormalities that include central obesity, insulin resistance, hyperinsulinemia, glucose intolerance, hypertension, dyslipidemia, hypercoagulability and an increased risk of coronary and cerebral vascular disease. These metabolic and vascular abnormalities are the main cause of cardiovascular mortality in western societies. Endothelial dysfunction, an early step in the development of atherosclerosis, has been reported in obese nondiabetic individuals and in patients with Type 2 diabetes. It has also been observed in individuals at high risk for Type 2 diabetes, including those with impaired glucose tolerance and the normoglycemic first-degree relatives of Type 2 diabetic patients. Recent evidence points to adipocytes as a complex and active endocrine tissue whose secretory products, including free fatty acids and several cytokines (i.e., leptin, adiponectin, tissue necrosis factor-alpha, interleukin-6, and resistin) play a major role in the regulation of human metabolic and vascular biology. These adipocytokines have been claimed to be the missing link between insulin resistance and cardiovascular disease. Interventions designed to improve endothelial and/or adipose-tissue functions may reduce cardiovascular events in obese individuals with either the metabolic syndrome or Type 2 diabetes. Lifestyle modification in the form of caloric restriction and increased physical activity are the most common modalities used for treating those individuals at risk and is unanimously agreed to be the initial step in managing Type 2 diabetes. Several recent studies have demonstrated favorable impacts of lifestyle modifications in improving endothelial function and insulin sensitivity, in addition to altering serum levels of adipocytokines and possibly reducing cardiovascular events. This review discusses current knowledge of the role of lifestyle modifications in ameliorating cardiovascular risk in obese subjects with either the metabolic syndrome or Type 2 diabetes.
Hamdy
Osama
O
Joslin Diabetes Center, Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA. Osama.Hamdy@joslin.harvard.edu
D000273:Adipose Tissue; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000517:prevention & control*; D016207:Cytokines / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000503:physiopathology / Q000628:therapy*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007328:Insulin / Q000502:physiology; D009765:Obesity / Q000150:complications* / Q000503:physiopathology / Q000628:therapy*; D012307:Risk Factors; D040242:Risk Reduction Behavior
D016207:Cytokines; D007328:Insulin