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Updated: Apr 18, 2026

Visualization of Endogenous Mitophagy Complexes In Situ in Human Pancreatic Beta Cells Utilizing Proximity Ligation Assay
Published on: May 2, 2019
Minireview: Autophagy in pancreatic β-cells and its implication in diabetes
Hirotaka Watada1, Yoshio Fujitani
1Department of Metabolism and Endocrinology (H.W., Y.F.), Centers for Molecular Diabetology (H.W., Y.F.) and Therapeutic Innovations in Diabetes (H.W.), and Japan Science and Technology Agency (JST)-CREST Program (Y.F.), Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
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.
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