| Background and Purpose: Spread worldwide, obesity, especially abdomen obesity, is often blended with hypertension, diabetes, hyperlipoidemia and many other risk factors of cardiovascular disease. Gathering in the body, they induce or exacerbate cardiovascular diseases and manifest themselves in metabolic syndrome. The research on obesity has aroused the attention of many people and scholars all over the world and has become a focus of research in the world of medical science. Animal model of obesity induced by food is still too unitary in terms of the types it can represent despite that it resembles human obesity. The model is often accompanied by weight gain and change in blood lipid but seldom by hypertension. Consequently, to better investigate the obese features and the pathogenesis of obesity, it is significant and urgent to develop a rat model of MS that can imitate the condition of human obesity and other metabolic disorders such as obesity, hypertension, etc.Renin–angiotensin system (RAS) is an important system that readjusts the balance between blood pressure and water electrolysis. Recent research has found that besides circulating RAS, tissues such as heart, blood vassal, brain, kidney and so on can also synthesize into AGT, rennin and ACE and in turn effectively become Ang II with an independent RAS system. Being able to secrete independently, laterally and locally, Ang II of this kind plays an important role in the pathological change of the organic growth, fibrosis and inflammatory response, etc. The combination of Ang II with AT1R can activate the signal pathways inside the cell, including Rho/ROCK and ERK/p38MAPK. The combination can mediate most biological effects of the RAS such as vascular contraction, rise in blood pressure, increase in aldehyde sterone, and restructuring, cell multiplication and cytomegalism, etc. It has been reported that there exists the expression of mRNA, the major component part of RAS, suggesting that the adipose tissues also contain some RAS in them. Recently, researchers have accepted that the increased RAS activity in the obese tissues probably plays an important role in the pathogenesis of obesity-related hypertension and affects the adipose tissue growth, but by what path they function remains to be investigated. Now the question is: do the various components of RAS system in the adipose tissues of obese humans express themselves in different ways? Does this have anything to do with the adipocyte hypertrophy and multiplication? Are the signal pathways inside the hypertrophic and multiplied adipocytes the same as that of other tissues in that they are also activated by way of Rho/ROCK and ERK/p38MAK? Or do different adipose tissues in different parts of the body vary in their respective signal pathways?In the present study, the pathogenic features of obesity population in China were investigated by a screening survey of obese subjects in community populations, with an aim at establishing an animal model of obesity closer to human obese features and investigating the pathophysiological role of adipose tissues such as RAS and RhoA/ ROCK, ERK/p38 signal pathways in the incidence of obesity and adipose tissues. Another purpose of this study is to find experimental data for a new method of prevention and treatment of obesity and MS.Methods: (1) Epidemiologic investigation: By field survey, 1449 subjects aged 30 or older were screened, including 730 males and 719 females. The investigation indexes: height, weight, blood pressure, waist circumference, hip circumference, waist-to-hip ratio, BMI and 75g dextrose tolerance test and FAT% assessment. Diagnostic indexes for obesity and overweight: standards of WHO, Asian-Pacific Region and adult Chinese BMI respectively. Diagnostic indexes for diabetes and hypertension: standard of WHO (1999). (2) Animal model research: 1. 30 normal 8-week-old male Wistar rats were equally randomized into 2 groups, the NC group and the MS group. MS rat models were duplicated by feeding food containing 49% high-fat and salt. 2. Blo...
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