Abstract
We generated the homozygous transgenic mice with expression of the active form of TGF-β1 by the glucagon promoter (homozygous NOD-TGF-β1). The homozygous NOD-TGF-β1 showed severe diabetes in 84.6%, impaired glucose tolerance, and low serum insulin levels. The final size of endocrine and whole pancreas decreased, respectively, to 6 and 34%, compared to wild-type mice. The homozygous N 2 backcross to C57BL/6 (B6-TGF-β1) showed no diabetes, but impaired glucose tolerance and low serum insulin levels. In homozygous NOD-TGF-β1, the expression of p15 INK4b was induced by 3.4-fold in pancreatic islets than that in wild-type mice. Based on these, we conclude first that excessive paracrine TGF-β1 signaling in islets results in endocrine and exocrine pancreatic hypoplasia, second that TGF-β1decrease the final size of endocrine and exocrine pancreas presumably through regulating cell cycle via p15 INK4b at least in endocrine pancreas, and third that hypoplastic action of TGF-β1 of pancreatic islets is independent of the genetic background.
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