Insulin receptor (IR)-deficient pups rapidly become hyperglycemic and hyperinsulinemic and die of diabetic ketoacidosis within a few days. Immunocytochemical analysis of the endocrine pancreas revealed that IR deficiency did not alter islet morphology or the number of beta-, alpha-, delta-, and pancreatic polypeptide (PP) cells. The lack of IR did not result in major changes in the expression of islet hormone genes or of beta-cell-specific marker genes encoding pancreas duodenum homeobox-containing transcription factor-1 (PDX-1), glucokinase (GCK), and GLUT2, as shown by reverse transcriptase-polymerase chain reaction analysis. The serum glucagon levels in IR-deficient and nondiabetic littermates were comparable. Finally, total insulin content in the pancreas of IR-deficient pups was gradually depleted, indicating sustained insulin secretion, not compensated for by increased insulin biosynthesis. These findings are discussed in light of recent results suggesting a role of IR in beta-cell function.
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Abstract| February 01 2001
Endocrine pancreas in insulin receptor-deficient mouse pups.
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M Jackerott, A Baudry, B Lamothe, D Bucchini, J Jami, R L Joshi; Endocrine pancreas in insulin receptor-deficient mouse pups.. Diabetes 1 February 2001; 50 (suppl_1): S146–9. https://doi.org/10.2337/diabetes.50.2007.S146
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