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Genetics, obesity, and the metabolic syndrome:The Professor Donald S. FredricksonMemorial Lecture

机译:遗传学,肥胖和代谢综合征:唐纳德教授S. FredRicksonmemorial讲座

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The metabolic syndiome consists of a clustering of metabolic lisk factors in one individual. These risk factors consist of atherogenic dyslipidemia (high triglyceiides, high apolipoprotein B [apo B], small LDL particles, and low HDL), elevated blood pressure, insulin resistance +- elevated plasma glucose, a prothrombotic state, and a proinflammatory state. Although the metabolic syndrome is increasingly common around the world and represents an important cause of cardiovascular disease (CVD), its pathogenesis is not well understood. The two major underlying causes appear to be obesity or other disorders of adipose tissue and insulin resistance.There is little doubt that genetic susceptibility plays an important role in the development of the metabolic syndrome. This paper addresses the question of the interaction between obesity and genetic susceptibility in the etiology of the metabolic syndrome Genetic susceptibility appears to exist at three levels: within adipose tissue itself, in insulin signaling pathways, and in regulation of individual risk factors. A major research challenge for the future is to unravel the complex genetic architecture that gives rise to the metabolic syndrome once a person becomes obese.
机译:代谢Syndiome由一个人中的代谢LISK因子组成。这些危险因素包括致动脉粥样血小胺血症(高阶段,高载脂蛋白B [APO B],小LDL颗粒和低HDL),血压升高,胰岛素抵抗+升高的血浆葡萄糖,普形癌态和促炎状态。虽然代谢综合征在世界各地越来越常见,但代表了心血管疾病(CVD)的重要原因,其发病机制尚不清楚。两种主要的潜在原因似乎是肥胖或脂肪组织和胰岛素抵抗的其他疾病。遗憾的是,遗传易感性在代谢综合征的发展中发挥着重要作用。本文解决了肥胖症与遗传敏感性之间的相互作用问题,在代谢综合征遗传易感性似乎存在于三个水平中:在脂肪组织本身,胰岛素信号传导途径,以及在个体危险因素的调节中。未来的主要研究挑战是解开复杂的遗传架构,一旦一个人变得肥胖,就会引起代谢综合征的复杂遗传建筑。

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