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Angiotensin (1-7) Improves Pancreatic Islet Function via Upregulating PDX-1 and GCK: A Dose-Dependent Study in Mice

Ziwei Lin1,2, Jiaqi Lin1,2, Anqi Huang1,2

  • 1Shantou University Medical College, Shantou, China.

International Journal of Endocrinology
|December 30, 2024
PubMed

Insights

Angiotensin (1-7) administration significantly improved glucose and lipid metabolism in db/db mice. This peptide enhanced islet function by increasing beta-cell ratios and promoting PDX-1 and GCK gene expression.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Molecular Biology

Background:

  • Type 2 diabetes is characterized by impaired insulin secretion and glucose intolerance.
  • The angiotensin system plays a role in metabolic regulation, with angiotensin (1-7) showing potential therapeutic benefits.

Purpose of the Study:

  • To investigate the effects of angiotensin (1-7) on islet function and glucose metabolism in a mouse model of type 2 diabetes.
  • To explore the underlying signaling pathways, including PDX-1 and GCK expression, involved in angiotensin (1-7) mediated improvements.

Main Methods:

  • db/db mice were treated with varying doses of angiotensin (1-7) for 8 weeks.
  • Evaluated changes in body weight, food intake, lipid metabolism, and glucose tolerance.
  • Assessed pancreatic islet morphology, beta-cell mass, and expression of PDX-1 and GCK.

Main Results:

  • Angiotensin (1-7) treatment, particularly at 600 μg/kg/d, reduced body weight, triglyceride levels, and fasting blood glucose.
  • Improved glucose tolerance and increased the proportion of beta cells and small islets.
  • Significantly upregulated PDX-1 and GCK gene expression in pancreatic tissue.

Conclusions:

  • Angiotensin (1-7) effectively improves glucose and lipid metabolism in db/db mice.
  • The peptide enhances islet function and beta-cell health.
  • Upregulation of PDX-1 and GCK expression is a key mechanism for angiotensin (1-7)'s beneficial effects.
Keywords:
GCKPDX-1angiotensin (1–7)diabetes mellitusislet cells

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