Hexosamine flux, the O-GlcNAc modification, and the development of insulin resistance in adipocytes
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 II diabetes. Adipose tissue-specific elevation in hexosamine flux in animal models recapitulates whole-body insulin-resistan...
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| Veröffentlicht in: | Molecular and cellular endocrinology 2010-04, Vol.318 (1), p.44-53 |
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| creator | Teo, Chin Fen Wollaston-Hayden, Edith E. Wells, Lance |
| description | 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 II 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. |
| doi_str_mv | 10.1016/j.mce.2009.09.022 |
| format | Article |
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| ispartof | Molecular and cellular endocrinology, 2010-04, Vol.318 (1), p.44-53 |
| issn | 0303-7207 1872-8057 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Acetylglucosamine - metabolism Adipocyte Adipocytes - physiology Adipocytokine Animals Biosynthesis Culture Elevation Flux Glucose Glycosylation Hexosamine biosynthesis pathway Hexosamines - metabolism Humans Insulin Insulin - pharmacology Insulin resistance Insulin Resistance - physiology Modulators O-GlcNAc modification Pathways |
| title | Hexosamine flux, the O-GlcNAc modification, and the development of insulin resistance in adipocytes |
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