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Updated: Jan 16, 2026

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
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I-BET151 modulates glucokinase gene expression and beta cell function in part through changes in FOXO1 expression.

Qing Wei Calvin Ho1, James A Miller1, Divya Gunaseelan1

  • 1Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Singapore, Republic of Singapore.

Diabetologia
|September 26, 2025
PubMed
Summary

BET inhibition may harm pancreatic beta cell function. This study found that I-BET151 reduced glucose regulation and insulin secretion in mice, impacting key beta cell genes. Caution is advised for BET inhibitor therapies.

Keywords:
BET protein inhibitorsBeta cellsEpigenetic modulatorsFOXO1GCKHNF4aI-BET151INS-1EMODYPancreatic islets

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Area of Science:

  • Epigenetics and molecular biology
  • Endocrinology and metabolism
  • Cancer biology

Background:

  • Bromodomain and extra-terminal (BET) proteins are epigenetic readers modulating gene transcription.
  • BET proteins are implicated in diseases like cancer and type 1 diabetes.
  • Potential off-target effects of BET inhibitors on host cells require investigation.

Purpose of the Study:

  • To investigate the secondary effects of BET inhibition on pancreatic beta cell function.
  • To determine the impact of the BET inhibitor I-BET151 on glucose homeostasis and insulin secretion.
  • To identify molecular mechanisms underlying BET inhibition's effects on beta cells.

Main Methods:

  • In vitro, ex vivo, and in vivo studies using the BET inhibitor I-BET151.
  • Glucose tolerance tests (GTTs) and insulin tolerance tests (ITTs) in mice.
  • Glucose-stimulated insulin secretion assays and transcriptomic analysis in rodent and human islets.

Main Results:

  • I-BET151 administration increased glucose excursions and reduced insulin responses in healthy and diabetic mice.
  • I-BET151 significantly decreased the expression of essential beta cell function genes (e.g., Hnf4α, Gck, Hnf1α, Glut2).
  • Transcriptomic analysis revealed downregulation of the PI3K-Akt pathway, with FOXO1 modulation partially rescuing effects.

Conclusions:

  • BET inhibition may have detrimental effects on pancreatic beta cell function.
  • High concentrations of BET inhibitors could negatively impact glucose regulation and insulin secretion.
  • Therapeutic use of BET inhibitors requires caution due to potential adverse effects on beta cells.