| Background and objective: Metabolic syndrome (MS) is a clustering character of cardiovascular multifactorial risk, Multifactorial cardiovascular risk are more harmful than only one factor. The environmental and inherited factors are believed to contribute to the etiology of MS, the onset of MS is complex ,its mechanism is not clear. It was recognized that insulin resistance was focus of MS.Peroxisome proliferator-activated receptors(PPARs) are ligand-inducible transcription factors that include PPARα, PPARδ and PPAR. PPARα is expressed mainly in tissues that have a high ratio of fatty acid(FA0) such as the liver, kidney, heart and muscle, PPARγis expressed mainly in fat, vascular endothelial cell and smooth muscle cell, PPARδis the most widely distributed subtype and is often expressed in heart and kidney at high levels. Now studies indicated PPARs involved in control of fatty acids oxidation,PPARα expression is significantly down-regulated during over-loaded left ventricular hypertrophy,this was associated with the down-regulation of several key enzymes of lipid metabolism, its synthetic ligands such as fibrates was able to improve lipid metabolism and atherosclerosis. PPARγ involved in adipose cell differentiation, PPARγ gene mutant may associated with type 2 diabetes and obesity. PPARγ activation by rosiglitazone results in improving type 2 diabetes ,obesity and insulin resistance, and lowering blood pressure. Little is known about the function of PPARδcompared with the others, the studies demonstrated PPARδ plays a central role in differentiation of preadipocytes and lipids metabolism, it involved in control of inflammatory status and atherosclerosis. Consequently PPARs plays a important role in regulating glucose and lipid metabolism, it may be one of key molecules associated with MS.It is not clear whether PPARs gene mutant may be associated with MS and cardiovascular phenotypes resulted from MS. Dose PPARs influence cardiovascular remodeling and function in MS and how? Epidemiology demonstrated excess fat intake and physical inactivity were major factors contributed to the onset of human obesity, diabetes and MS, especially the mechanism of MS induced by diet and physical activity remains to be explored thoroughly. Now the models of type 2 diabetes and obesity have been established, but those models do not have all human character of MS, animal models of MS are few. In the study, rat model of MS resembling human trait of MS is established, the purpose of this study is to explore the role of PPARs in cardiovascular remodeling and dysfunction, little is known. Material and Methods: In order to study relationship between PPARs gene polymorphism and cardiovascular phenotypes in the patients with MS, and the role of PPARs in cardiovascular remodeling and dysfunction in MS.Clinical studies: According to MS criterion made by WHO in 1999,hypertension criterion by WHO/ISH in 1999 and type 2 diabetes criterion by ADA in 1997,we studied 623 patients and 134 normal controls , 304 of all cases suffered from MS(age: 59±13 years for 160 men and 144 women), 172 patients(age: 56±12 years for 92 men and 80 women) were diagnosed with essential hypertension (EH), 147 patients were diagnosed with type 2 diabetes (age: 54±11 years for 85 men and 62 women) and 134 controls (age: 55±9 years for 92 men and 42 women). Polymerase chain reaction-restricted fragments length polymorphism was used to study the PPARγC161-T,PPARδ+294T/C and PPAR α intron 7 Polymorphism, fasting insulin(FINS),fasting blood glucose(FBG),uric Acid (UA),plasma lipids and urinary albumin excretion(UAE) were examined, ultrasonography for carotid intimal-media thickness and plaque indices and Doppler echocardiography for left ventricular parameters were examined.Experimental studies: Sixty Wistar male rats were randomed at 2 months of age into four groups: one group received normal chow(NC), the others high-fat feeding(HF) group, normal chow plus exercise(NCE)group and high-fat feeding plus exercise(HFE)group respectively, he high...
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