Protective mechanism of glucose against alloxan-induced pancreatic beta-cell damage

Biochem Biophys Res Commun. 1995 May 5;210(1):1-6. doi: 10.1006/bbrc.1995.1619.

Abstract

Glucose prevented the alloxan- or H2O2-induced inhibition of insulin secretion in rat pancreatic islets. Hydrogen peroxide was detected during the incubation of islets with alloxan, and this generation of hydrogen peroxide was not affected by glucose. Treatment of beta-cells with alloxan or H2O2 caused elevation of cytosolic free Ca2+ and decrease of cellular NAD+. Glucose blocked the decrease of cellular NAD+ level, but did not abolish the increase of cytosolic Ca2+. These results indicate that glucose protected pancreatic beta-cell damage after the H2O2 generation and Ca2+ influx on a chain of reactions in the diabetogenesis of alloxan.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alloxan / antagonists & inhibitors*
  • Animals
  • Calcium / metabolism
  • Diabetes Mellitus, Experimental / chemically induced*
  • Glucose / pharmacology*
  • Hydrogen Peroxide / metabolism
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / drug effects*
  • Male
  • NAD / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors

Substances

  • Insulin
  • NAD
  • Alloxan
  • Hydrogen Peroxide
  • Glucose
  • Calcium