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Updated: Feb 13, 2026

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GPR142 prompts glucagon-like Peptide-1 release from islets to improve β cell function

Hua V Lin1, Jingru Wang2, Jie Wang2

  • 1Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.

Molecular Metabolism
|March 7, 2018
PubMed
Abstract

Insights

GPR142 agonists enhance insulin secretion and beta cell function. This study reveals GPR142

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Diabetes Research

Background:

  • G protein-coupled receptor 142 (GPR142) agonists are investigated for type 2 diabetes due to insulin-stimulating properties.
  • The precise roles of GPR142 within pancreatic islets beyond insulin secretion remain largely unexplored.

Purpose of the Study:

  • To investigate the broader functions of GPR142 in pancreatic islet cells.
  • To elucidate the mechanisms underlying GPR142's effects on islet cell function and survival.

Main Methods:

  • In situ hybridization and immunostaining to determine GPR142 expression patterns in pancreatic islets.
  • Treatment of human and mouse islets with a selective GPR142 agonist.
  • Assessment of glucagon and insulin secretion, prohormone convertase 1/3 (PC1/3) expression, and beta cell proliferation and apoptosis.

Main Results:

  • GPR142 is expressed in both alpha (α) and beta (β) cells.
  • GPR142 stimulation increases glucagon secretion and enhances glucagon-like peptide-1 (GLP-1) production and release via PC1/3 upregulation.
  • GPR142-mediated insulin secretion and content increase depend on intact GLP-1 receptor signaling; GPR142 also promotes β cell proliferation and protects islets from apoptosis.

Conclusions:

  • Local GLP-1 release from α cells is a key mediator of GPR142's beneficial effects on β cell function and mass.
  • GPR142 agonism demonstrates potential for treating type 2 diabetes through improved β cell function and survival.
  • GPR142 activation offers a promising therapeutic strategy for type 2 diabetes management.
Keywords:
GPR142Intra-islet GLP-1PC1/3α cell

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