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Diabetes: Compound Stops Islet Destruction

  September, 5 2001 19:27
your information resource in human molecular genetics
Type I diabetes, in which the beta cells of the pancreas produce too little or no insulin, accounts for 3% of all new cases of diabetes each year. While the routine treatment for this disease is injections of insulin, an international team of scientists may have discovered a potentially new therapy for the condition (Nature Medicine, Vol. 7, No. 9, Sep 01).

One feature of Type 1 diabetes is a decrease in the number of Natural Killer T (NKT) cells of the immune system. This deficit also occurs in a mouse model of diabetes known as the NOD, or non-obese diabetic mouse model. The compound alpha-galactosylceramide (a-GalCer), binds to receptors on NKT-cells called CD1d receptors, and stimulates the production of cytokines from NKT-cells.

When they administered a-GalCer to NOD mice, the scientists found that it protected mice from developing diabetes even when given after onset of insulitis, and prolonged the survival of insulin-producing pancreatic islets transplanted into newly diabetic mice. In addition, a-GalCer enhanced the response to, and production of, vital cytokines by NKT cells.

The authors propose that a-GalCer decreases the destruction of islet cells by the body's own immune system and may have beneficial effects in diabetic patients.


Dr. Terry Delovitch
Department of Microbiology and Immunology
University of Western Ontario
London, Ontario, Canada
Tel: +1 519-663-3972
Fax: +1 519-663-3847
Email: del@rri.on.ca

Dr. Jean-François Bach
Institut National de la Santé
Centre de l'Association Claude Bernard
Hôpital Necker
61 rue de Sèvres
Paris Cedex 15, France
Tel: +33 1 444 9 5371
Fax: +33 1 4306 2388
E-mail: bach@necker.fr

Dr. Luc Van Kaer
Howard Hughes Medical Institute
Department of Microbiology and Immunology
Vanderbilt University School of Medicine
Nashville, Tennessee
Tel: +1 615 343 2707
Fax: +1 615 343 2972
Email: vankael@ctrvax.vanderbilt.edu

(C) Nature Medicine press release.

Message posted by: Trevor M. D'Souza

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