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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Autophagy modulators in type 2 diabetes: A new perspective.

Ayah Talal Zaidalkilani1, Hayder M Al-Kuraishy2, Esraa H Fahad3

  • 1Department of Nutrition, Faculty of Pharmacy and Medical Sciences, University of Petra, Amman, Jordan.

Journal of Diabetes
|December 16, 2024
PubMed
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Autophagy influences type 2 diabetes (T2D) by affecting insulin secretion and sensitivity. Modulating autophagy with inhibitors or activators may offer therapeutic strategies for T2D.

Keywords:
autophagyinsulin resistancetype 2 diabetes mellitusβ‐cells

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Area of Science:

  • Cellular Biology
  • Metabolic Disorders
  • Endocrinology

Background:

  • Type 2 diabetes (T2D) involves impaired insulin signaling and secretion.
  • Autophagy, a cellular degradation process, plays a complex role in T2D pathogenesis.
  • Dysfunctional autophagy contributes to pancreatic beta-cell impairment and insulin resistance.

Purpose of the Study:

  • To review the dual role of autophagy in T2D.
  • To explore the therapeutic potential of autophagy modulators in T2D.

Main Methods:

  • Literature review of autophagy's role in T2D.
  • Analysis of studies on autophagy inhibitors and activators in T2D models.

Main Results:

  • Basal autophagy supports pancreatic beta-cell function and insulin sensitivity.
  • Overactivated autophagy can lead to beta-cell apoptosis and dysfunction.
  • Autophagy's role in T2D is context-dependent, acting as a double-edged sword.

Conclusions:

  • Autophagy modulation presents a potential therapeutic avenue for T2D.
  • Targeting autophagy with inhibitors or activators warrants further investigation for T2D treatment.