Deficiency of Adiponectin Receptor 2 Reduces Diet-Induced Insulin Resistance but Promotes Type 2 Diabetes
Author(s) -
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,
Anne ReifelMiller
Publication year - 2006
Publication title -
endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.674
H-Index - 257
eISSN - 1945-7170
pISSN - 0013-7227
DOI - 10.1210/en.2006-0708
Subject(s) - medicine , endocrinology , insulin resistance , adiponectin , type 2 diabetes , insulin , diabetes mellitus , adiponectin receptor 1 , receptor
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 β-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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