Obesity and insulin resistance
Obesity and insulin resistance
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DOI：
10.1172/jci10842
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发表时间：
2000-08-01
影响因子：
15.9
通讯作者：
Flier, JS
中科院分区：
文献类型：
--
作者：
Kahn, BB;Flier, JS
肥胖与2型糖尿病的关系已经被认识了几十年，这种联系的主要基础是肥胖能够产生胰岛素抵抗。胰岛素抵抗是2型糖尿病病因学的一个基本方面，也与广泛的其他病理生理后遗症有关，包括高血压、高脂血症、动脉粥样硬化（即代谢综合征或X综合征）和多囊卵巢疾病（1）。虽然肥胖症的脂肪组织质量增加导致全身胰岛素抵抗的机制的许多细节仍然未知，但过去几年我们对现在可能被称为脂肪-胰岛素轴的理解有了爆炸性的增长。也有理由认为，胰岛素抵抗和高胰岛素血症除了由肥胖引起外，还可能导致肥胖的发展。在这一视角中，我们将回顾最近的进展，强调有争议或不确定的领域，并提出澄清未决问题的方法。
The association of obesity with type 2 diabetes has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance. Insulin resistance is a fundamental aspect of the etiology of type 2 diabetes and is also linked to a wide array of other pathophysiologic sequelae including hypertension, hyperlipidemia, atherosclerosis (ie, the metabolic syndrome, or syndrome X), and polycystic ovarian disease (1). Although many details of the mechanisms by which the enlarged adipose tissue mass that defines obesity causes systemic insulin resistance remain unknown, the past several years have witnessed an explosive increase in our understanding of what may now be referred to as the adipo-insulin axis. There are also grounds for considering the related possibility that insulin resistance and hyperinsulinemia, in addition to being caused by obesity, can contribute to the development of obesity. In this Perspective, we will review recent progress, highlight areas of controversy or uncertainty, and suggest approaches to clarifying the unresolved issues.