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Updated: Dec 25, 2025

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Beta cell identity changes with mild hyperglycemia: Implications for function, growth, and vulnerability

Aref G Ebrahimi1, Jennifer Hollister-Lock1, Brooke A Sullivan1

  • 1Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, One Joslin Place, Harvard Medical School, Boston, MA 02215, USA.

Molecular Metabolism
|April 4, 2020
PubMed
Abstract

Insights

Even mild glucose elevations in early diabetes disrupt beta cell function. Gene expression changes in pancreatic islets indicate adverse effects on insulin secretion, cell growth, and vulnerability.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • Diabetes mellitus is characterized by impaired insulin secretion and hyperglycemia.
  • The precise mechanisms by which early-stage hyperglycemia affects pancreatic beta cell function remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of mild glucose elevations on beta cell differentiation and function.
  • To identify molecular changes in pancreatic islets associated with early diabetes.

Main Methods:

  • Induction of mild hyperglycemia in rats via 90% partial pancreatectomy.
  • Analysis of gene expression in pancreatic islets using RNA sequencing at 4 and 10 weeks post-surgery.

Main Results:

  • Significant alterations in gene expression profiles of pancreatic islets were observed.
  • Downregulation of key genes for insulin secretion and upregulation of suppressed genes.
  • Changes in genes related to cell replication, aging, senescence, stress, inflammation, and MHC antigen expression.

Conclusions:

  • Mild hyperglycemia in early diabetes induces detrimental phenotypic changes in beta cells.
  • These changes adversely impact beta cell function, proliferation, and susceptibility to damage.
  • Early glycemic control is crucial for preserving beta cell health in diabetes.
Keywords:
DiabetesGlucose toxicityInsulin secretionPancreatic beta cellRNAseq

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