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Publication : Glucokinase gene locus transgenic mice are resistant to the development of obesity-induced type 2 diabetes.

First Author  Shiota M Year  2001
Journal  Diabetes Volume  50
Issue  3 Pages  622-9
PubMed ID  11246883 Mgi Jnum  J:67749
Mgi Id  MGI:1931361 Doi  10.2337/diabetes.50.3.622
Citation  Shiota M, et al. (2001) Glucokinase gene locus transgenic mice are resistant to the development of obesity-induced type 2 diabetes. Diabetes 50(3):622-9
abstractText  Transgenic mice that overexpress the entire glucokinase (GK) gene locus have been previously shown to be mildly hypoglycemic and to have improved tolerance to glucose. To determine whether increased GK might also prevent or diminish diabetes in diet-induced obese animals, we examined the effect of feeding these mice a high-fat high-simple carbohydrate low-fiber diet (HF diet) for 30 weeks. In response to this diet, both normal and transgenic mice became obese and had similar BMIs (5.3 +/- 0.1 and 5.0 +/- 0.1 kg/m2 in transgenic and non-transgenic mice, respectively). The blood glucose concentration of the control mice increased linearly with time and reached 17.0 +/- 1.3 mmol/l at the 30th week. In contrast, the blood glucose of GK transgenic mice rose to only 9.7 +/- 1.2 mmol/l at the 15th week, after which it returned to 7.6 +/- 1.0 mmol/l by the 30th week. The plasma insulin concentration was also lower in the GK transgenic animals (232 +/- 79 pmol/l) than in the controls (595 +/- 77 pmol/l), but there was no difference in plasma glucagon concentrations. Together, these data indicate that increased GK levels dramatically lessen the development of both hyperglycemia and hyperinsulinemia associated with the feeding of an HF diet.
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