Format

Send to

Choose Destination
Cell Rep. 2018 Nov 13;25(7):1708-1717.e5. doi: 10.1016/j.celrep.2018.10.040.

Autophagy Ablation in Adipocytes Induces Insulin Resistance and Reveals Roles for Lipid Peroxide and Nrf2 Signaling in Adipose-Liver Crosstalk.

Author information

1
Division of Endocrinology Diabetes and Metabolism, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
2
Department of Nutrition and Integrative Physiology, University of Utah College of Health and Program in Molecular Medicine, Salt Lake City, UT 84112, USA.
3
Division of Endocrinology Diabetes and Metabolism, University of Utah School of Medicine, Salt Lake City, UT 84112, USA; Progenitor Life Sciences, Salt Lake City, UT 84108, USA. Electronic address: tim.graham@progenitorlifesciences.com.
4
Department of Nutrition and Integrative Physiology, University of Utah College of Health and Program in Molecular Medicine, Salt Lake City, UT 84112, USA. Electronic address: sihem.boudina@u2m2.utah.edu.

Abstract

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 mitochondrial 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.

KEYWORDS:

adipocytes; adiponectin; adipose tissue; autophagy; inflammation; insulin resistance; lipid peroxide; mitochondria

PMID:
30428342
DOI:
10.1016/j.celrep.2018.10.040
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center