The role of endoplasmic reticulum stress in nonimmune diabetes: NOD.k iHEL, a novel model of β cell death

L. Socha, D. Silva, S. Lesage, C. Goodnow, N. Petrovsky

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

The final common pathway in diabetes development is β cell apoptosis. We herein describe a novel diabetes model based on transgenic NOD.k iHEL mice, wherein male mice develop diabetes due to nonimmune-mediated β cell death. Histology and electron microscopy confirm endoplasmic reticulum (ER) abnormalities that are consistent with endoplasmic stress caused by the HEL transgene. The NOD.k iHEL model may be particularly useful for studying mechanisms of β cell death secondary to ER stress and also for testing potential therapies designed to protect β cells from stress-induced apoptosis. The observation that only male NOD.k iHEL mice develop diabetes and exhibit ER abnormalities is intriguing and suggests these mice may be useful in deciphering the link between hyperandrogenism, insulin resistance, and diabetes.

Original languageEnglish
Pages (from-to)178-183
Number of pages6
JournalAnnals of the New York Academy of Sciences
Volume1005
Issue number1
DOIs
Publication statusPublished - 1 Nov 2003
Externally publishedYes

Keywords

  • Cell death
  • Diabetes
  • Endoplasmic reticulum (ER) stress
  • NOD.k iHEL
  • β cell

Fingerprint Dive into the research topics of 'The role of endoplasmic reticulum stress in nonimmune diabetes: NOD.k iHEL, a novel model of β cell death'. Together they form a unique fingerprint.

Cite this