Streptozotocin-Induced Diabetes Increases γ-Glutamyltranspeptidase Activity but not Expression in Rat Liver

John B. Watkins, James E. Klaunig, Heather M. Smith, Paul Cornwell, Ruth A. Sanders

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Earlier work describing increased biliary excretion of the acetaminophen-cysteine conjugate advanced the hypothesis that streptozotocin-induced diabetes increases γ-glutamyltranspeptidase (GGT) expression in Sprague-Dawley rats. To test this hypothesis, rats were divided into control, diabetic, and insulin-treated diabetic groups. Diabetes was induced by intravenous injection of 45 mg streptozotocin/kg body weight and was effectively controlled by insulin treatment in the appropriate group. Densitometric quantification demonstrated that hepatic GGT activity in diabetic rats was significantly increased when compared to normal and insulin-treated diabetic controls. Histochemical staining of liver was greater in female than in male rats, and staining increased in female rat liver as the duration of diabetes lengthened from 30 to 90 days. GGT activity was increased by diabetes in liver canalicular-enriched and basolateral-enriched membrane preparations, and it was unchanged in renal brush border-enriched membranes. Total mRNA isolated from diabetic and insulin-treated diabetic rat livers did not conclusively demonstrate an elevation of GGT mRNA relative to normal. Western blot analysis showed no differences in the amount of GGT in diabetic versus normal rat livers. These data indicate that streptozotocin-induced diabetes does not alter the expression of, but does increase the activity of, GGT in liver.

Original languageEnglish (US)
Pages (from-to)219-225
Number of pages7
JournalJournal of Biochemical and Molecular Toxicology
Issue number4
StatePublished - 1998


  • Gamma-Glutamyltranspeptidase
  • Insulin-Dependent Diabetes Mellitus
  • Liver
  • Rats
  • Streptozotocin

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Health, Toxicology and Mutagenesis
  • Toxicology

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