Islet neogenesis associated protein transgenic mice are resistant to hyperglycemia induced by streptozotocin
0301 basic medicine
Pancreatic Elastase
Gene Expression
Proteins
Mice, Transgenic
Pancreatitis-Associated Proteins
Immunohistochemistry
Immunity, Innate
Diabetes Mellitus, Experimental
12. Responsible consumption
Mice
03 medical and health sciences
Insulin-Secreting Cells
Models, Animal
Animals
Insulin
In Situ Hybridization
DOI:
10.1677/joe.1.06698
Publication Date:
2006-09-26T19:33:29Z
AUTHORS (6)
ABSTRACT
Islet neogenesis associated protein (INGAP) is a protein factor that can stimulate new islet mass from adult pancreatic progenitor cells. In models of islet neogenesis, INGAP expression is elevated in pancreatic acinar cells. Using a transgenic model to drive a sustained expression of INGAP in pancreatic acinar cells, we have identified a protection to chemical-induced hyperglycemia. A sustained expression of INGAP during development did not perturb islet development or basal blood glucose homeostasis, although β-cell mass and pancreatic insulin content were significantly increased in the INGAP transgenic mice. When challenged with a diabetogenic dose of streptozotocin (STZ), mice carrying the INGAP transgene did not become hyperglycemic. In contrast, wild-type mice became and remained hyperglycemic, blood glucose > 550 mg/dl. The serum insulin levels and islet morphology were preserved in the transgenic mice after STZ treatment. These data suggest that the sustained expression of INGAP in the acinar pancreas confers resistance to a diabetogenic insult. The INGAP transgenic mouse provides a new model to uncover factors that are protective to diabetes onset and biomarkers to track β-cell pathology.
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