期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 318, 期 1-2, 页码 44-53出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2009.09.022
关键词
Hexosamine biosynthesis pathway; O-GlcNAc modification; Insulin resistance; Adipocyte; Adipocytokine
资金
- NIH/NIDDK [1RO1DK075069]
Excess flux through the hexosamine biosynthesis pathway in adipocytes is a fundamental cause of glucose toxicity and the development of insulin resistance that leads to type H diabetes. Adipose tissue-specific elevation in hexosamine flux in animal models recapitulates whole-body insulin-resistant phenotypes, and increased hexosamine flux in adipocyte cell culture models impairs insulin-stimulated glucose uptake. Many studies have been devoted to unveiling the molecular mechanisms in adipocytes in response to excess hexosamine flux-mediated insulin resistance. As a major downstream event consuming and incorporating the final product of the hexosamine biosynthesis pathway, dynamic and inducible O-GlcNAc modification is emerging as a modulator of insulin sensitivity in adipocytes. Given that O-GlcNAc is implicated in both insulin-mediated signal transduction and transcriptional events essential for adipocytokine secretion, direct functional studies to pinpoint the roles of O-GlcNAc in the development of insulin resistance via excess flux through hexosamine biosynthesis pathway are needed. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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