Pajvani Utpal B, Scherer Philipp E
Department of Cell Biology and Diabetes Research and Training Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Curr Diab Rep. 2003 Jun;3(3):207-13. doi: 10.1007/s11892-003-0065-2.
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. Many 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.
脂肪细胞特异性分泌分子,即脂肪因子,打破了脂肪组织仅仅是脂质惰性储存库的观念,并突出了其作为一个活跃的内分泌器官的作用,该器官监测并改变全身代谢,维持能量稳态。这些脂肪因子之一,脂联素(也称为Acrp30、AdipoQ和GBP28),最近作为胰岛素敏感性的介质受到了极大关注。过去几年的许多临床报告和基因研究表明,在人类和动物模型的代谢功能障碍(如肥胖和胰岛素抵抗)中,这种激素的循环水平会降低。在啮齿动物中进行的脂联素药物治疗可提高胰岛素敏感性,尽管其主要作用部位和详细作用机制尚待确定。脂联素缺乏和转基因脂联素过量产生动物模型的表型强调了脂联素在维持葡萄糖和脂质稳态中的作用。