Minireview: Autophagy in pancreatic β-cells and its implication in diabetes

Mol Endocrinol. 2015 Mar;29(3):338-48. doi: 10.1210/me.2014-1367. Epub 2015 Jan 29.

Abstract

Autophagy is a conserved system for the degradation of cytoplasmic proteins and organelles. During insulin resistance, in which insulin secretion is enhanced and β-cell mass is increased owing to changes in the expression and function of various proteins in pancreatic β-cells, autophagic activity appears to also be enhanced to adapt to the dynamic changes occurring in β-cells. Indeed, defective autophagy in β-cells recapitulates several features that are observed in islets during the development of type 2 diabetes mellitus. In addition, the dyregulation of autophagic activity appears to occur in the β-cells of type 2 diabetic model mice and type 2 diabetes mellitus patients. These lines of evidence suggest that autophagic failure may be implicated in the pathophysiology of type 2 diabetes mellitus. In this review, we summarized the recent findings regarding how autophagy in β-cells is regulated and how dysfunction of the autophagic machinery may lead to the dysfunction of β-cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autophagy*
  • Diabetes Mellitus / pathology*
  • Endoplasmic Reticulum Stress
  • Fatty Acids / metabolism
  • Humans
  • Insulin-Secreting Cells / pathology*
  • Mitophagy

Substances

  • Fatty Acids

Grants and funding

This work was supported by The Ministry of Education, Sports and Culture of Japan Grants 23390244, 26293220, and 26111518 (to H.W.) and 22590996 (to Y.F.), Daiichi-Sankyo Foundation of Life Science (H.W. and Y.F.), and the UBE Foundation (H.W.).