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Role for Oxidative Stress in the Regeneration of Islet Beta Cells?
  1. Kathryn Haskins,
  2. Jennifer Kench,
  3. Katherine Powers,
  4. Brenda Bradley,
  5. Subbiah Pugazhenthi,
  6. Jane Reusch,
  7. Marcia McDuffie
  1. From the Departments of Immunology (K.H., J.K., K.P., B.B.) and Medicine (S.P., J.R.), University of Colorado Health Sciences Center, Denver, CO; Departments of Microbiology and Internal Medicine (M.M.), University of Virginia, Charlottesville, VA.
  1. Address correspondence to: Dr. Kathryn Haskins, Department of Immunology, UCHSC/NJMRC, 1400 Jackson Street, Denver, CO 80206; E-mail: katie.haskins{at}uchsc.edu.
  2. Presented in part at the American Federation for Medical Research-sponsored symposium during Experimental Biology 2003: Translating the Genome, San Diego, CA, April 11-15, 2003.

Abstract

In the nonobese diabetic (NOD) mouse model of type 1 diabetes, we have found that there are increased markers of oxidative stress in islet beta cells in prediabetic animals when compared with control strains. Treatment of these mice with a superoxide dismutase (SOD) mimetic can markedly reduce the level of nitrotyrosine found in islets. In a diabetes-resistant NOD congenic mouse, the NOD.Lc7 mouse, we found increased beta cell proliferation and decreased apoptosis in islets. There are also lower levels of nitrotyrosine in islets of NOD.Lc7 mice than in NOD mice, suggesting that NOD.Lc7 islets are less susceptible to oxidative damage. We hypothesize that there may be a link between the ability of islet cells to regenerate and their resistance to oxidative stress.

Key Words
  • oxidative stress
  • islet regeneration

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