| First Author | Terauchi Y | Year | 1995 |
| Journal | J Biol Chem | Volume | 270 |
| Issue | 51 | Pages | 30253-6 |
| PubMed ID | 8530440 | Mgi Jnum | J:30334 |
| Mgi Id | MGI:77846 | Doi | 10.1074/jbc.270.51.30253 |
| Citation | Terauchi Y, et al. (1995) Pancreatic beta-cell-specific targeted disruption of glucokinase gene. Diabetes mellitus due to defective insulin secretion to glucose. J Biol Chem 270(51):30253-6 |
| abstractText | Mice carrying a null mutation in the glucokinase (GK) gene in pancreatic beta-cells, but not in the liver, were generated by disrupting the beta-cell-specific exon. Heterozygous mutant mice showed early-onset mild diabetes due to impaired insulin-secretory response to glucose. Homozygotes showed severe diabetes shortly after birth and died within a week. GK-deficient islets isolated from homozygotes showed defective insulin secretion in response to glucose, while they responded to other secretagogues: almost normally to arginine and to some extent to sulfonylureas. These data provide the first direct proof that GK serves as a glucose sensor molecule for insulin secretion and plays a pivotal role in glucose homeostasis. GK-deficient mice serve as an animal model of the insulin-secretory defect in human non-insulin-dependent diabetes mellitus. |
