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Ghrelin Improves Glucolipotoxicity-Induced Pancreatic β-Cellular Dysfunction and Apoptosis by Inhibiting Endoplasmic

Xin-Ying Li1,2, Chun-Rong Zhong1, Jin-Chan Wu1

  • 1Medical Care Center, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, 570311 Haikou, Hainan, China.

Discovery Medicine
|July 26, 2024
PubMed
Abstract

Insights

Ghrelin protects pancreatic beta cells from glucolipotoxicity by reducing endoplasmic reticulum stress and improving insulin secretion. This peptide shows potential as a therapeutic agent for beta-cell dysfunction and diabetes.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Diseases

Background:

  • Glucolipid toxicity in pancreatic beta cells contributes to diabetes development.
  • Endoplasmic reticulum stress (ERS) is a key factor in this cellular dysfunction.
  • Ghrelin, a pancreatic peptide, has shown a negative correlation with oxidative stress.

Purpose of the Study:

  • To investigate the role of ghrelin in protecting against glycolipid-induced beta-cell dysfunction.
  • To elucidate the underlying mechanisms of ghrelin's protective effects.

Main Methods:

  • Mouse insulinoma NIT-1 cells were subjected to high glucose and high fat to induce glucolipotoxicity.
  • Cells were treated with acylated ghrelin (AG).
  • Apoptosis, cell viability, insulin synthesis/secretion, and the IRE1/JNK signaling pathway were assessed.

Main Results:

  • Ghrelin treatment enhanced NIT-1 cell viability and reduced apoptosis.
  • Ghrelin promoted insulin synthesis and secretion.
  • Ghrelin attenuated endoplasmic reticulum stress and inhibited the IRE1/JNK signaling pathway.

Conclusions:

  • Ghrelin ameliorates beta-cell dysfunction caused by glucolipotoxicity.
  • The protective mechanism involves the inhibition of ERS-induced IRE1/JNK signaling.
  • Ghrelin presents a potential therapeutic strategy for beta-cell dysfunction.
Keywords:
IRE1/JNK signaling pathwayghrelinglucolipidβ-cellular dysfunction

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