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Deficiency of Adiponectin Receptor 2 Reduces Diet-Induced Insulin Resistance but Promotes Type 2 Diabetes

Type 2 Diabetes Drug Hunting Team (Y.L., M.D.M., K.A.O., K.W.S., A.R.-M.), Atherosclerosis Drug Hunting Team (W.R.B.), and Discovery Pathology (S.K.S., J.M.S.), Lilly Research Laboratories, Indianapolis, Indiana 46285; Deltagen, Inc. (S.K.), San Carlos, California 94070; and Isis Pharmaceuticals (B.P.M., S.F.M., S.B.), Carlsbad, California 92008

Address all correspondence and requests for reprints to: Anne Reifel Miller, Ph.D., Type 2 Diabetes Drug Hunting Team, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285. E-mail: a.r.miller{at}lilly.com.

Adiponectin/adiponectin receptors (AdipoR) are involved in energy homeostasis and inflammatory pathways. To investigate the role of AdipoR2 in metabolic control, we studied the lipid and glucose metabolic phenotypes in AdipoR2-deficient mice. AdipoR2 deletion diminished high-fat diet-induced dyslipidemia and insulin resistance yet deteriorated glucose homeostasis as high-fat feeding continued, which resulted from the failure of pancreatic ß-cells to adequately compensate for the moderate insulin resistance. A defect in the AdipoR2 gene may represent a mechanism underlying the etiology of certain subgroups of type 2 diabetic patients who eventually develop overt diabetes, whereas other obese patients do not.

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