期刊
BIOCHIMIE
卷 94, 期 10, 页码 2131-2136出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biochi.2012.01.017
关键词
Adiponectin; Muscle; Liver; Insulin sensitivity; Obesity
Adiponectin administration improves glucose tolerance in rodents. This is due to both reductions in hepatic glucose production, and likely improved insulin stimulated glucose disposal in skeletal muscle. Adiponectin's effects in both liver and muscle are believed to be due in large part to AMP-activated protein kinase (AMPK) activation, resulting in a reduction in hepatic gluconeogenic enzymes and increased fatty acid oxidation and reduced ectopic lipid deposition in muscle. In addition, adiponectin can robustly stimulate mitochondria] biogenesis, at least in muscle, and this appears to be due to AMPK-independent mechanisms. Various treatments successful at improving insulin response (thiazolidinediones (TZDs), n-3 polyunsaturated fatty acid (PUFA) supplementation) also stimulate adiponectin production. Obesity and insulin resistance are often characterized by both a state of resistance to adiponectin (both liver and muscle), as well as a reduction in total circulating adiponectin concentrations. The mechanisms underlying the impaired response of muscle and liver to adiponectin have not been clearly elucidated. Surprisingly, the significance of adiponectin resistance, at least in muscle, is not entirely clear. While the development of adiponectin resistance precedes intramuscular lipid accumulation and impaired insulin response in high-fat fed rodents, the restoration of adiponectin response does not appear to be necessary in order to restore insulin response in muscle. Further research examining the cellular mechanisms underlying the development of adiponectin resistance, and the importance of treating this, needs to be conducted. (C) 2012 Elsevier Masson SAS. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据