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This version published online on October 26, 2006
Endocrinology, doi:10.1210/en.2006-0708
A more recent version of this article appeared on February 1, 2007
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Submitted on May 25, 2006
Accepted on October 17, 2006

Deficiency of AdipoR2 Reduces Diet-induced Insulin Resistance, Yet Promotes Type 2 Diabetes

Yanfang Liu, M. Dodson Michael, Shera Kash, William R. Bensch, Brett P. Monia, Susan F. Murray, Keith A. Otto, Samreen K. Syed, Sanjay Bhanot, Kyle W. Sloop, John M. Sullivan, and Anne Reifel-Miller*

Type 2 Diabetes Drug Hunting Team, Atherosclerosis Drug Hunting Team, and Discovery Pathology, Lilly Research laboratories, Indianapolis, Indiana 46285; Deltagen, Inc. San Carlos, California 94070; Isis Pharmaceuticals, Carlsbad, California 92008

* To whom correspondence should be addressed. E-mail: a.r.miller{at}lilly.com.

Adiponectin/adiponectin receptors 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 {beta} 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 while other obese patients do not.
Key words: Adiponectin receptor 2 • type 2 diabetes • insulin resistance • high fat diet • obesity • dyslipidemia • beta cell




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R. S. Ahima and M. A. Lazar
Adipokines and the Peripheral and Neural Control of Energy Balance
Mol. Endocrinol., May 1, 2008; 22(5): 1023 - 1031.
[Abstract] [Full Text] [PDF]


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