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This Article Full Text Full Text (PDF) A corrigendum has been published All Versions of this Article: 292/5/E1301    most recent 00312.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Li, W. Articles by Hawkins, M. Search for Related Content PubMed PubMed Citation Articles by Li, W. Articles by Hawkins, M.

Insulin-sensitizing effects of thiazolidinediones are not linked to adiponectin receptor expression in human fat or muscle

Departments of Medicine, Surgery, and Cell Biology, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, New York

Submitted 28 June 2006 ; accepted in final form 3 January 2007

Circulating adiponectin levels are increased by the thiazolidinedione (TZD) class of PPAR agonists in concert with their insulin-sensitizing effects. Two receptors for adiponectin (AdipoR1 and AdipoR2) are widely expressed in many tissues, but their physiological significance to human insulin resistance remains to be fully elucidated. We examined the expression patterns of AdipoR1 and AdipoR2 in fat and skeletal muscle of human subjects, their relationship to insulin action, and whether they are regulated by TZDs. Expression patterns of both AdipoRs were similar in subcutaneous and omental fat depots, with higher expression in adipocytes than in stromal cells and macrophages. To determine the effects of TZDs on AdipoR expression, subcutaneous fat and quadriceps muscle were biopsied in 14 insulin-resistant subjects with type 2 diabetes mellitus after 45 mg pioglitazone or placebo for 21 days. This duration of pioglitazone improved insulin's suppression of glucose production by 41% and enhanced stimulation of glucose uptake by 27% in concert with increased gene expression and plasma levels of adiponectin. Pioglitazone did not affect AdipoR expression in muscle, whole fat, or cellular adipose fractions, and receptor expression did not correlate with baseline or TZD-enhanced insulin action. In summary, both adiponectin receptors are expressed in cellular fractions of human fat, particularly adipocytes. TZD administration for sufficient duration to improve insulin action and increase adiponectin levels did not affect expression of AdipoR1 or AdipoR2. Although TZDs probably exert many of their effects via adiponectin, changes in these receptors do not appear to be necessary for their insulin-sensitizing effects.

insulin resistance; diabetes mellitus; adipose tissue