Transgenic mice expressing IFN-γ in pancreatic β-cells are resistant to streptozotocin-induced diabetes

D. Gu, M. Arnush, S. P. Sawyer, N. Sarvetnick

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


In 28 adult Ins-IFN-γ transgenic mice, injection of high doses of streptozotocin (STZ; first injection, 300 μg/g body weight; second injection, 200 μg/g body weight 4 h later) failed to induce severe hyperglycemia. To the contrary, 28 BALB/c mice developed diabetes mellitus after identical injections of STZ. Because the STZ-induced islet damage was partially inhibited in Ins-IFN-γ transgenic mice, their glycemia levels became normal 4 days after STZ administration. Both transgenic and BALB/c mice lost weight after receiving STZ, but the body weights of transgenic mice then returned to pretreatment levels in a nearly parallel manner with the glycemia. Immunolabeling with insulin identified an unusual spreading pattern of insulin immunoreactivity. Ultrastructural observations confirmed that β- cell necrosis and degranulation were more severe in STZ-treated BALB/c than in Ins-IFN-γ transgenic mice. Moreover, regeneration of pancreatic duct cells and islet neogenesis were observed in the transgenic mice. Therefore, after STZ treatment, the Ins-IFN-γ transgenic mice apparently were resistant to the induction of severe diabetes, whereas their BALB/c age-matched counterparts succumbed to the disease.

Original languageEnglish (US)
Pages (from-to)E1089-E1094
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number6 32-6
StatePublished - 1995
Externally publishedYes


  • pancreas
  • pancreatic ductal cell

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


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