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Endocrinology Vol. 143, No. 3 998-1007
Copyright © 2002 by The Endocrine Society

INSULIN-GLUCAGON-GI PEPTIDES-DIABETES MELLITUS

Induction of Adipocyte Complement-Related Protein of 30 Kilodaltons by PPAR{gamma} Agonists: A Potential Mechanism of Insulin Sensitization

Terry P. Combs, John A. Wagner, Joel Berger, Tom Doebber, Wen-Jun Wang, Bei B. Zhang, Michael Tanen, Anders H Berg, Stephen O’Rahilly, David B. Savage, Krishna Chatterjee, Stuart Weiss, Patrick J. Larson, Keith M. Gottesdiener, Barry J. Gertz, Maureen J. Charron, Philipp E. Scherer and David E. Moller

Departments of Cell Biology (T.P.C., A.H.B., P.E.S.) and Biochemistry (W.-H.W., M.J.C.) Albert Einstein College of Medicine, Bronx, New York 10461; Departments of Molecular Endocrinology (J.B., T.D., B.B.Z., M.T., D.E.M.), Clinical Pharmacology (J.A.W., K.M.G., B.J.G.), and Clinical Biostatistics and Research Data Systems (P.J.L.), Merck Research Laboratories, Rahway, New Jersey 07065; Departments of Medicine and Clinical Biochemistry (S.O’R., D.B.S., K.C.), University of Cambridge, Addenbrooke’s Hospital, Cambridge CB2 2QQ, United Kingdom; and San Diego Endocrine and Metabolic Clinic (S.W.), San Diego, California 92108

Address all correspondence and requests for reprints to: Philipp Scherer, Albert Einstein College of Medicine, Chanin 414, Department of Cell Biology, 1300 Morris Park Avenue, Bronx, New York 10461. E-mail: . scherer{at}aecom.yu.edu

Adipocyte complement-related protein of 30 kDa (Acrp30, adiponectin, or AdipoQ) is a fat-derived secreted protein that circulates in plasma. Adipose tissue expression of Acrp30 is lower in insulin-resistant states and it is implicated in the regulation of in vivo insulin sensitivity. Here we have characterized the ability of PPAR{gamma} agonists to modulate Acrp30 expression. After chronic treatment of obese-diabetic (db/db) mice with PPAR{gamma} agonists (11 d), mean plasma Acrp30 protein levels increased (>3x). Similar effects were noted in a nongenetic type 2 diabetes model (fat-fed and low-dose streptozotocin-treated mice). In contrast, treatment of mice (db/db or fat-fed) with metformin or a PPAR{alpha} agonist did not affect plasma Acrp30 protein levels. In a cohort of normal human subjects, 14-d treatment with rosiglitazone also produced a 130% increase in circulating Acrp30 levels vs. placebo. In addition, circulating Acrp30 levels were suppressed 5-fold in patients with severe insulin resistance in association with dominant-negative PPAR{gamma} mutations. Thus, induction of adipose tissue Acrp30 expression and consequent increases in circulating Acrp30 levels represents a novel potential mechanism for PPAR{gamma}-mediated enhancement of whole-body insulin sensitivity. Furthermore, Acrp30 is likely to be a biomarker of in vivo PPAR{gamma} activation.




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