Journal of Diabetes (Dec 2024)

Autophagy modulators in type 2 diabetes: A new perspective

  • Ayah Talal Zaidalkilani,
  • Hayder M. Al‐kuraishy,
  • Esraa H. Fahad,
  • Ali I. Al‐Gareeb,
  • Yaser Hosny Ali Elewa,
  • Mahmoud Hosny Zahran,
  • Athanasios Alexiou,
  • Marios Papadakis,
  • Ammar AL‐Farga,
  • Gaber El‐Saber Batiha

DOI
https://doi.org/10.1111/1753-0407.70010
Journal volume & issue
Vol. 16, no. 12
pp. n/a – n/a

Abstract

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Abstract Type 2 diabetes (T2D) is a chronic metabolic disorder caused by defective insulin signaling, insulin resistance, and impairment of insulin secretion. Autophagy is a conserved lysosomal‐dependent catabolic cellular pathway involved in the pathogenesis of T2D and its complications. Basal autophagy regulates pancreatic β‐cell function by enhancing insulin release and peripheral insulin sensitivity. Therefore, defective autophagy is associated with impairment of pancreatic β‐cell function and the development of insulin rersistance (IR). However, over‐activated autophagy increases apoptosis of pancreatic β‐cells leading to pancreatic β‐cell dysfunction. Hence, autophagy plays a double‐edged sword role in T2D. Therefore, the use of autophagy modulators including inhibitors and activators may affect the pathogenesis of T2D. Hence, this review aims to clarify the potential role of autophagy inhibitors and activators in T2D.

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