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Ann Endocrinol (Paris). 2004 Feb;65(1 Suppl):S36-43.

[Adiponectin: from adipocyte to skeletal muscle].

[Article in French]

Author information

1
INSERM U465, Centre de Recherches Biomédicales des Cordeliers, F-75270 Paris Cedex 06. pferre@bhdc.jussieu.fr

Abstract

Insulin resistance is characterized by a peripheral resistance to insulin-mediated glucose uptake, and an hepatic resistance of glucose production to insulin. Insulin resistance in skeletal muscle is of a particular importance, and could be the consequence of an increase in intracellular and circulating fatty acids and triglycerides. Adipose tIssue plays an important role to regulate mobilization and release of fatty acids. Adipose tIssue is an endocrine organ which secretes several factors, including adiponectin. Adiponectin improves insulin sensitivity in skeletal muscle and liver, through a stimulation of fatty acid oxidation and glucose utilization. Thiazolidinediones enhance adiponectin expression and synthesis through PPARgamma, although the precise mechanism remains controversial. AMP-activated protein kinase (AMPK) is the main adiponectin target. Adiponectin, clearly, is a major modulator of glucose and lipid metabolism in insulin-sensitive tIssue and/or regulator of insulin-sensitivity, in obese and/or glucose intolerant subjects, as well as in type 2 diabetes mellitus. Recent works and the links between insulin resistance, adipose tIssue, adiponectin and its PPARgamma-enhanced secretion are reviewed in this paper.

PMID:
15163922
[Indexed for MEDLINE]
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