| First Author | Dai C | Year | 2005 |
| Journal | Am J Pathol | Volume | 167 |
| Issue | 2 | Pages | 429-36 |
| PubMed ID | 16049329 | Mgi Jnum | J:99948 |
| Mgi Id | MGI:3584289 | Doi | 10.1016/s0002-9440(10)62987-2 |
| Citation | Dai C, et al. (2005) {beta}-Cell-Specific Ablation of the Hepatocyte Growth Factor Receptor Results in Reduced Islet Size, Impaired Insulin Secretion, and Glucose Intolerance. Am J Pathol 167(2):429-36 |
| abstractText | Hepatocyte growth factor (HGF) and its c-met receptor consist of a paired signaling system that has been implicated in the regulation of pancreatic beta-cell survival, proliferation, and function. To define the role of HGF/c-met signaling in beta-cell biology in vivo, we have generated conditional knockout mice in which the c-met receptor gene was specifically inactivated in pancreatic beta cells by the Cre-loxP system. Mice with beta-cell-specific deletion of the c-met receptor (betamet(-/-)) displayed slight growth retardation, mild hyperglycemia, and decreased serum insulin levels at 6 months of age when compared with their control littermates. Deficiency of the c-met receptor in beta cells resulted in a complete loss of acute-phase insulin secretion in response to glucose and an impaired glucose tolerance. Glucose transporter-2 expression was down-regulated in the beta cells of betamet(-/-) mice. Compared to controls, betamet(-/-) mice exhibited reduced islet size and decreased insulin content in the pancreas, but displayed normal islet morphology. Therefore, HGF/c-met signaling plays an imperative role in controlling islet growth, in regulating beta-cell function, and in maintaining glucose homeostasis. |
