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Modeling diabetic alpha cell dysfunction using stem cell-derived alpha cells.

Swikriti Shrestha1, Lauren T Jennings1, Kyle Knofczynski1

  • 1Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, 200 1st Street SW, Rochester, MN 55902, USA.

Stem Cell Reports
|May 9, 2025
PubMed
Summary
This summary is machine-generated.

Stem cell-derived alpha cells exposed to endoplasmic reticulum stress mimic diabetic dysfunction, including glucagon hypersecretion. A tyrosine kinase inhibitor, sunitinib, protected these cells, offering a new model for diabetes research.

Keywords:
GLP-1PC1/3PC2PCSK1PCSK2SC-α cellsglicentinglucagonglucagon-like peptide-1proglucagon processingprohormone convertase 1prohormone convertase 2stem cell-derived alpha cells

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Diabetes Research

Background:

  • Pancreatic alpha cell dysfunction is central to diabetes pathophysiology.
  • Diabetic alpha cells exhibit glucagon hypersecretion, altered proglucagon processing, and transcriptomic changes.
  • A lack of in vitro human alpha cell models hinders research into these defects.

Purpose of the Study:

  • To investigate the impact of endoplasmic reticulum (ER) stress on stem cell-derived alpha (SC-α) cells.
  • To establish a functional in vitro model for studying diabetic alpha cell phenotypes.
  • To identify potential therapeutic targets for correcting alpha cell dysfunction.

Main Methods:

  • Induction of ER stress in stem cell-derived alpha (SC-α) cells.
  • Measurement of glucagon and related peptide secretion (glicentin, GLP-1).
  • Analysis of transcriptomic profiles and key pathway expression (MAFB, glycolysis, oxidative phosphorylation).
  • Treatment of SC-α cells with sunitinib, a tyrosine kinase inhibitor.

Main Results:

  • ER stress in SC-α cells induced glucagon hypersecretion.
  • ER stress increased glicentin secretion and glucagon-like peptide-1 (GLP-1) expression.
  • ER stress led to a diabetic transcriptional state, downregulating MAFB and metabolic pathways.
  • Sunitinib treatment protected SC-α cells from ER stress-induced glucagon hypersecretion.

Conclusions:

  • ER stress in SC-α cells recapitulates key features of diabetic alpha cell dysfunction.
  • The SC-α cell model provides a platform for studying diabetes pathophysiology.
  • Sunitinib shows potential in protecting against ER stress-mediated alpha cell dysfunction.