Journal
CELL REPORTS
Volume 25, Issue 7, Pages 1708-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.10.040
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Funding
- United States National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [1-R01-DK-098646-01A1, R01-DK-099110]
- United States American Heart Association [16GRNT30990018, 15POST25360014]
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Autophagy is a homeostatic cellular process involved in the degradation of long-lived or damaged cellular components. The role of autophagy in adipogenesis is well recognized, but its role in mature adipocyte function is largely unknown. We show that the autophagy proteins Atg3 and Atg16L1 are required for proper mitochondria! function in mature adipocytes. In contrast to previous studies, we found that post-developmental ablation of autophagy causes peripheral insulin resistance independently of diet or adiposity. Finally, lack of adipocyte autophagy reveals cross talk between fat and liver, mediated by lipid peroxide-induced Nrf2 signaling. Our data reveal a role for autophagy in preventing lipid peroxide formation and its transfer in insulin-sensitive peripheral tissues.
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