Adiponectin: Systemic contributor to insulin sensitivity

被引：192
作者：
Utpal B. Pajvani
Philipp E. Scherer
机构：
[1] Department of Cell Biology, Diabetes Research/Training Center, Albert Einstein College of Medicine, Bronx, NY 10461
来源：
Current Diabetes Reports | 2003年 / 3卷 / 3期
基金：
美国国家卫生研究院;
关键词：
Insulin Resistance; Insulin Sensitivity; Adiponectin Level; Troglitazone; Adiponectin Expression;
D O I：
10.1007/s11892-003-0065-2
中图分类号：
学科分类号：
摘要：
Adipocyte-specific secreted molecules, termed adipokines, have dispelled the notion of adipose tissue as an inert storage depot for lipids, and highlighted its role as an active endocrine organ that monitors and alters whole-body metabolism and maintains energy homeostasis. One of these adipokines, adiponectin (also known as Acrp30, AdipoQ, and GBP28), has gained significant attention recently as a mediator of insulin sensitivity. Marty clinical reports and genetic studies over the past few years demonstrate decreased circulating levels of this hormone in metabolic dysfunction, such as obesity and insulin resistance, in both humans and animal models. Pharmacologic adiponectin treatments in rodents increase insulin sensitivity, although the primary site and detailed mechanism of action is yet to be determined. The phenotypes of adiponectin-deficient and transgenic adiponectin-overproducing animal models underscore the role of adiponectin in the maintenance of glucose and lipid homeostasis. Copyright © 2003 by Current Science Inc.
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收藏
页码：207 / 213
页数：6
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