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Cell Rep. 2021 May 25;35(8):109184. doi: 10.1016/j.celrep.2021.109184.

The autophagy protein Becn1 improves insulin sensitivity by promoting adiponectin secretion via exocyst binding.

Cell reports

Kenta Kuramoto, Yoon-Jin Kim, Jung Hwa Hong, Congcong He

Affiliations

  1. Department of Cell and Developmental Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
  2. Department of Cell and Developmental Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: [email protected].

PMID: 34038729 PMCID: PMC8177967 DOI: 10.1016/j.celrep.2021.109184

Abstract

Autophagy dysregulation is implicated in metabolic diseases, including type 2 diabetes. However, the mechanism by which the autophagy machinery regulates metabolism is largely unknown. Autophagy is generally considered a degradation process via lysosomes. Here, we unveil a metabolically important non-cell-autonomous, non-degradative mechanism regulated by the essential autophagy protein Becn1 in adipose tissue. Upon high-fat diet challenge, autophagy-hyperactive Becn1

Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.

Keywords: AMPK; Becn1; Sec6; adiponectin; adipose tissue; autophagy; exocyst; glucose tolerance; insulin sensitivity

Conflict of interest statement

Declaration of interests The authors declare no competing interests.

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