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Am J Physiol Endocrinol Metab 269: E1089-E1094, 1995;
0193-1849/95 $5.00
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AJP - Endocrinology and Metabolism, Vol 269, Issue 6 E1089-E1094, Copyright © 1995 by American Physiological Society

ARTICLES

Transgenic mice expressing IFN-gamma in pancreatic beta-cells are resistant to streptozotocin-induced diabetes

D. Gu, M. Arnush, S. P. Sawyer and N. Sarvetnick
Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037, USA.

In 28 adult Ins-IFN-gamma transgenic mice, injection of high doses of streptozotocin (STZ; first injection, 300 microgram/g body weight; second injection, 200 microgram/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-gamma 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 beta-cell necrosis and degranulation were more severe in STZ-treated BALB/c than in Ins-IFN-gamma transgenic mice. Moreover, regeneration of pancreatic duct cells and islet neogenesis were observed in the transgenic mice. Therefore, after STZ treatment, the Ins-IFN-gamma transgenic mice apparently were resistant to the induction of severe diabetes, whereas their BALB/c age-matched counterparts succumbed to the disease.


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