| First Author | Lu D | Year | 2005 |
| Journal | Mol Cell Biol | Volume | 25 |
| Issue | 15 | Pages | 6570-7 |
| PubMed ID | 16024793 | Mgi Jnum | J:100017 |
| Mgi Id | MGI:3586392 | Doi | 10.1128/MCB.25.15.6570-6577.2005 |
| Citation | Lu D, et al. (2005) Abnormal glucose homeostasis and pancreatic islet function in mice with inactivation of the fem1b gene. Mol Cell Biol 25(15):6570-7 |
| abstractText | Type 2 diabetes mellitus is a disorder of glucose homeostasis involving complex gene and environmental interactions that are incompletely understood. Mammalian homologs of nematode sex determination genes have recently been implicated in glucose homeostasis and type 2 diabetes mellitus. These are the Hedgehog receptor Patched and Calpain-10, which have homology to the nematode tra-2 and tra-3 sex determination genes, respectively. Here, we have developed Fem1b knockout (Fem1b-KO) mice, with targeted inactivation of Fem1b, a homolog of the nematode fem-1 sex determination gene. We show that the Fem1b-KO mice display abnormal glucose tolerance and that this is due predominantly to defective glucose-stimulated insulin secretion. Arginine-stimulated insulin secretion is also affected. The Fem1b gene is expressed in pancreatic islets, within both beta cells and non-beta cells, and is highly expressed in INS-1E cells, a pancreatic beta-cell line. In conclusion, these data implicate Fem1b in pancreatic islet function and insulin secretion, strengthening evidence that a genetic pathway homologous to nematode sex determination may be involved in glucose homeostasis and suggesting novel genes and processes as potential candidates in the pathogenesis of diabetes mellitus. |
