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Intracellular pathways of pancreatic β-cell apoptosis in type 1 diabetes

Helen E Thomas1, Thomas W Kay

  • 1St Vincent's Institute of Medical Research, Department of Medicine, University of Melbourne, St Vincent's Hospital, Fitzroy, Melbourne, Victoria, Australia. hthomas@svi.edu.au

Diabetes/Metabolism Research and Reviews
|November 10, 2011
PubMed
Abstract

Insights

Bid protein protects beta cells from diabetes-related damage. Targeting Bid may prevent beta cell death in type 1 diabetes and islet transplantation. This research clarifies apoptosis pathways in diabetes.

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Immunology

Background:

  • Beta cell apoptosis is a hallmark of type 1 diabetes.
  • Beta cell loss is also observed in type 2 diabetes and islet graft rejection.

Purpose of the Study:

  • To investigate intracellular pathways regulating beta cell apoptosis in diabetes.
  • To examine the role of Bid, a pro-apoptotic Bcl-2 family member, in beta cell death.
  • To identify Bcl-2 family molecules involved in killing induced by high glucose concentrations.

Main Methods:

  • Studied intracellular pathways regulating beta cell apoptosis in type 1 and type 2 diabetes.
  • Utilized islets from Bid-deficient mice to assess Bid's role.
  • Investigated Bcl-2 family molecules involved in cell death induced by high glucose or ribose.

Main Results:

  • Bid-deficient islets showed protection against perforin, granzyme B, and Fas-mediated killing.
  • Bid deficiency offers a potential therapeutic target for protecting beta cells from type 1 diabetes insults.
  • Islets lacking Bim or Puma, but not Bid, were protected from glucose toxicity.

Conclusions:

  • Different stimuli activate distinct initiator molecules within the Bcl-2-regulated apoptosis pathway in beta cells.
  • Bid plays a crucial role in mediating beta cell apoptosis induced by immune and cytotoxic insults relevant to type 1 diabetes.
  • Bim and Puma are key mediators of glucose-induced beta cell toxicity.

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