Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 486, Issue 1, Pages 88-93Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2009.02.017
Keywords
3T3-L1; Glucose uptake; Insulin resistance; Reactive oxygen species; Uncoupling protein
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Funding
- National Basic Research Program of China [2004CB720000, 2006CB911001]
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Uncoupling protein 2 (UCP2) was reported to be involved in insulin-glucose homeostasis, based on well established event that inhibition of UCP2 stimulates insulin secretion in pancreatic p-cells. However, the role of UCP2 on insulin-stimulated glucose uptake in adipose tissue, which is an indispensable process in insulin-glucose homeostasis, remains unknown. In this study, UCP2 was inhibited by genipin in 3T3-L1 adipocytes, which increased mitochondrial membrane potential, intracellular ATP level and production of reactive oxygen species (ROS). Importantly, insulin-stimulated glucose uptake in 3T3-L1 adipocytes was largely impaired in the presence of genipin, and recovered by CCCP, a mitochondrial uncoupler. Furthermore, genipin leaded to suppression of insulin signal transduction through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptor substrate-1 (IRS-1). These results suggest that mitochondrial uncoupling in adipocytes positively regulates insulin-stimulated glucose uptake in adipocytes, and UCP2 may play an important role in insulin resistance. (C) 2009 Elsevier Inc. All rights reserved.
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