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Trends Cell Biol. 2016 May;26(5):341-351. doi: 10.1016/j.tcb.2016.01.002. Epub 2016 Jan 25.

Nuclear Mechanisms of Insulin Resistance.

Author information

1
Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Current address: Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA, USA.
2
Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
3
Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. Electronic address: erosen@bidmc.harvard.edu.

Abstract

Insulin resistance is a sine qua non of type 2 diabetes and is associated with many other clinical conditions. Decades of research into mechanisms underlying insulin resistance have mostly focused on problems in insulin signal transduction and other mitochondrial and cytosolic pathways. By contrast, relatively little attention has been focused on transcriptional and epigenetic contributors to insulin resistance, despite strong evidence that such nuclear mechanisms play a major role in the etiopathogenesis of this condition. In this review, we summarize the evidence for nuclear mechanisms of insulin resistance, focusing on three transcription factors with a major impact on insulin action in liver, muscle, and fat.

PMID:
26822036
PMCID:
PMC4844850
DOI:
10.1016/j.tcb.2016.01.002
[Indexed for MEDLINE]
Free PMC Article

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