| First Author | Jackerott M | Year | 2001 |
| Journal | Diabetes | Volume | 50 Suppl 1 |
| Pages | S146-9 | PubMed ID | 11272177 |
| Mgi Jnum | J:67190 | Mgi Id | MGI:1930035 |
| Doi | 10.2337/diabetes.50.2007.s146 | Citation | Jackerott M, et al. (2001) Endocrine pancreas in insulin receptor-deficient mouse pups. Diabetes 50 Suppl 1:S146-9 |
| abstractText | 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. |
