Journal
TRENDS IN CELL BIOLOGY
Volume 26, Issue 5, Pages 341-351Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2016.01.002
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Funding
- NIDDK NIH HHS [R01 DK085171, T32 DK007516, R01 DK102173, R01 DK102170] Funding Source: Medline
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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 mitochondria! 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.
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