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Updated: Jan 21, 2026

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
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SIRT1 Activation Promotes β-Cell Regeneration by Activating Endocrine Progenitor Cells via AMPK Signaling-Mediated

Shang Ying Wu1, Juan Liang1, Bao Chen Yang1

  • 1School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.

Stem Cells (Dayton, Ohio)
|August 11, 2019
PubMed

Insights

Sirtuin 1 (SIRT1) activation promotes beta-cell regeneration in diabetes models by stimulating new endocrine progenitor cells. This process involves AMP-activated protein kinase (AMPK) signaling and fatty acid oxidation (FAO).

Area of Science:

  • Endocrinology
  • Stem Cell Biology
  • Metabolic Regulation

Background:

  • Diabetes treatment strategies focus on beta-cell regeneration.
  • Calorie restriction influences tissue regeneration, including beta cells, through metabolic pathways.
  • Sirtuin 1 (SIRT1) is a key mediator of calorie restriction's effects.

Purpose of the Study:

  • To investigate the potential of SIRT1 activation for stimulating beta-cell regeneration.
  • To elucidate the mechanisms underlying SIRT1-mediated beta-cell regeneration.

Main Methods:

  • SIRT1 activation using SRT1720 in streptozotocin (STZ)-induced beta-cell-deficient neonatal rats.
  • Analysis of neurogenin3 (NGN3)-positive endocrine progenitor activation.
  • Assessment of SIRT1 expression during beta-cell regeneration and mouse pancreas development.
  • In vitro studies using cultured pancreatic rudiments and human pancreatic progenitor cells.
  • Investigation of AMP-activated protein kinase (AMPK) signaling and fatty acid oxidation (FAO) pathways.

Main Results:

  • SRT1720 treatment promoted beta-cell regeneration in STZ-induced rats.
  • Regeneration was driven by activation of NGN3-positive endocrine progenitors from ductal cells.
  • SIRT1 activation upregulated endocrine progenitor differentiation in vitro.
  • SIRT1-induced NGN3 upregulation was mediated by AMPK signaling and fatty acid oxidation (FAO).

Conclusions:

  • SIRT1 activation effectively promotes beta-cell restoration and endocrine progenitor differentiation.
  • The mechanism involves the regulation of AMPK signaling-mediated fatty acid oxidation (FAO).
  • SIRT1 represents a potential therapeutic target for diabetes treatment via beta-cell regeneration.
Keywords:
DiabetesEndocrine progenitorsMetabolismNGN3Pancreas developmentPancreatic ductal cellsSIRT1β-Cell regeneration

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