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Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based

Safia Costes1, Gyslaine Bertrand1, Magalie A Ravier1

  • 1IGF, Univ. Montpellier, CNRS, INSERM, 34094 Montpellier, France.

International Journal of Molecular Sciences
|June 2, 2021
PubMed

Insights

Type 2 diabetes involves beta-cell dysfunction and loss. This review explores how amyloid, fat, and sugar trigger beta-cell death and how therapies may protect them.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Cell Biology

Background:

  • Type 2 diabetes (T2D) features chronic hyperglycemia due to declining pancreatic beta-cell function and insulin resistance.
  • Reduced beta-cell mass, often from apoptosis, contributes significantly to T2D pathophysiology.
  • Diabetogenic factors like amyloid deposits, lipotoxicity, and glucotoxicity induce beta-cell apoptosis.

Purpose of the Study:

  • To review the molecular mechanisms underlying pancreatic beta-cell apoptosis in diabetes-prone conditions.
  • To explore signaling pathways targeted by glucagon-like peptide-1 (GLP-1) therapies for beta-cell protection.

Main Methods:

  • Literature review of molecular mechanisms in beta-cell apoptosis.
  • Analysis of signaling pathways involved in GLP-1-based therapeutic strategies.

Main Results:

  • Identified key molecular pathways driving beta-cell apoptosis under lipotoxicity, glucotoxicity, and amyloid stress.
  • Highlighted the role of GLP-1 receptor agonists in activating protective signaling cascades.

Conclusions:

  • Understanding beta-cell apoptosis mechanisms is crucial for T2D pathogenesis.
  • GLP-1-based therapies show promise in protecting beta-cells from apoptosis in T2D contexts.
Keywords:
GLP-1apoptosisglucotoxicityislet amyloidisletslipotoxicitypancreatic beta-cells

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