| First Author | Epstein PN | Year | 1992 |
| Journal | Proc Natl Acad Sci U S A | Volume | 89 |
| Issue | 24 | Pages | 12038-42 |
| PubMed ID | 1465437 | Mgi Jnum | J:97924 |
| Mgi Id | MGI:3576689 | Doi | 10.1073/pnas.89.24.12038 |
| Citation | Epstein PN, et al. (1992) Expression of yeast hexokinase in pancreatic beta cells of transgenic mice reduces blood glucose, enhances insulin secretion, and decreases diabetes. Proc Natl Acad Sci U S A 89(24):12038-42 |
| abstractText | It has been proposed that endogenous hexokinases of the pancreatic beta cell control the rate of glucose-stimulated insulin secretion and that genetic defects that reduce beta-cell hexokinase activity may lead to diabetes. To test these hypotheses, we have produced transgenic mice that have a 2-fold increase in hexokinase activity specific to the pancreatic beta cell. This increase was sufficient to significantly augment glucose-stimulated insulin secretion of isolated pancreatic islets, increase serum insulin levels in vivo, and lower the blood glucose levels of transgenic mice by 20-50% below control levels. Elevation of hexokinase activity also significantly reduced blood glucose levels of diabetic mice. These results confirm the role of beta-cell hexokinase activity in the regulation of insulin secretion and glucose homeostasis. They also provide strong support for the proposal that reductions in beta-cell hexokinase activity can produce diabetes. |
