Deficiency of adiponectin receptor 2 reduces diet-induced insulin resistance but promotes type 2 diabetes

被引：93

作者：

Liu, Yanfang

Michael, M. Dodson

Kash, Shera

Bensch, William R.

Monia, Brett P.

Murray, Susan F.

Otto, Keith A.

Syed, Samreen K.

Bhanot, Sanjay

Sloop, Kyle W.

Sullivan, John M.

Reifel-Miller, Anne ^{[1
]}

机构：

[1] Eli Lilly & Co, Lilly Res Labs, Type 2 Diabet Drug Hunting Team, Indianapolis, IN 46285 USA

[2] Lilly Res Labs, Atherosclerosis Drug Hunting Team, Indianapolis, IN 46285 USA

[3] Lilly Res Labs, Discovery Pathol, Indianapolis, IN 46285 USA

[4] Deltagen Inc, San Carlos, CA 94070 USA

[5] ISIS Pharmaceut, Carlsbad, CA 92008 USA

来源：

ENDOCRINOLOGY | 2007年 / 148卷 / 02期

关键词：

D O I：

10.1210/en.2006-0708

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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 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, whereas other obese patients do not.

引用

收藏

页码：683 / 692

页数：10

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