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Isolated Pancreatic Islet Treatment and Apoptosis Measurement
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Isolated Pancreatic Islet Treatment and Apoptosis Measurement

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Pancreatic islets from type 2 diabetic patients have functional defects and increased apoptosis that are ameliorated

Piero Marchetti1, Silvia Del Guerra, Lorella Marselli

  • 1Department of Endocrinology and Metabolism and Diabetes, Transplant Unit, University of Pisa, Italy. marchant@immr.med.unipi.it.

The Journal of Clinical Endocrinology and Metabolism
|November 9, 2004
PubMed

Insights

Metformin improves pancreatic beta-cell function and survival in type 2 diabetes (T2D) by reducing oxidative stress. This study shows metformin ameliorates T2D islet defects, enhancing insulin secretion and reducing apoptosis.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Diabetes Research

Background:

  • Type 2 diabetes (T2D) is associated with pancreatic beta-cell dysfunction and increased apoptosis.
  • Oxidative stress plays a significant role in the pathogenesis of T2D beta-cell failure.
  • Metformin is known to protect non-diabetic beta-cells, but its direct effects on T2D islets require investigation.

Purpose of the Study:

  • To investigate the functional and survival defects of pancreatic beta-cells in T2D.
  • To determine the direct effects of metformin on T2D islet cells.
  • To elucidate the role of oxidative stress in T2D beta-cell dysfunction and metformin's mechanism of action.

Main Methods:

  • Isolation of islets from T2D subjects.
  • Assessment of insulin content, insulin mRNA expression, and insulin granule characteristics.
  • Measurement of glucose-induced insulin secretion and apoptosis markers (caspase-3, -8).
  • Evaluation of oxidative stress markers (nitrotyrosine, NADPH oxidase, antioxidant enzymes).
  • Incubation of T2D islets with metformin and subsequent analysis.

Main Results:

  • T2D islets exhibited reduced insulin content, impaired secretion, decreased insulin mRNA, increased apoptosis, and elevated oxidative stress.
  • Metformin treatment of T2D islets increased insulin content, improved insulin secretion and mRNA levels, and reduced apoptosis.
  • Metformin significantly reduced markers of oxidative stress in T2D islets.
  • Enhanced insulin granule number and density were observed after metformin treatment.

Conclusions:

  • Pancreatic beta-cells in T2D display significant functional and survival deficits, linked to oxidative stress.
  • Metformin demonstrates direct beneficial effects on T2D islet cells, improving function and survival.
  • The protective effects of metformin in T2D are, at least partially, mediated through the reduction of oxidative stress.

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