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Lab Reports
January 1, 2014

Newly Discovered Mechanism Points to Diabetes Prevention Strategy

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Copyright 2013 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

JAMA. 2014;311(1):19. doi:10.1001/jama.2013.285448

New research reveals that the immune attack that occurs with type 1 diabetes compromises functioning of the endoplasmic reticulum (ER), the structure within cells that folds and packages proteins and lipids. This reduced ER function results in ER stress and contributes to the death of insulin-producing beta cells, according to a study by Harvard School of Public Health investigators and their colleagues (Engin F et al. Sci Transl Med. 2013;5[211]:211ra156).

Previous research showed that ER stress can be corrected with “chemical chaperones” such as taurine-conjugated ursodeoxycholic acid (TUDCA), a bile acid. In this study, applying TUDCA to mouse models of type 1 diabetes improved ER and beta cell function. Also, diabetes-prone mice that were treated with TUDCA had a dramatically reduced incidence of type 1 diabetes. TUDCA is an approved drug for certain cases of liver disease, and it is linked with no major adverse effects.

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