Impaired glucose tolerance and mild hyperglycemia in sucrose-fed rats does not impair insulin secretion.

We fed normal rats a high sucrose diet in order to test the hypothesis that mild hyperglycemia can induce defects in pancreatic beta-cell function and impair glucose-stimulated insulin release. Rats provided with free access to a sucrose solution (35%) voluntarily consumed 50% more carbohydrate than control per day. After 7 days of sucrose feeding, glucose tolerance was significantly impaired; the area under the glucose tolerance test curve (GTT) was 683 +/- 61 mmol/120 min compared with 472 +/- 56 mmol/120 min in controls (P < 0.05). Impaired glucose tolerance was still present after a further 12 days (area under the GTT: 749 +/- 99 mmol/120 min). Sucrose-fed rats were significantly (P < 0.05) hyperglycemic by 1.5 mmol/l over controls. When insulin secretion was assessed in vivo and in vitro in control and sucrose-fed rats, no significant differences were apparent in plasma samples collected over a 1-h period or in statically incubated or perifused isolated pancreatic islets. In addition, the rates of glucose utilisation and oxidation were normal in islets from sucrose-fed rats. These data do not support the hypothesis that minimal hyperglycemia is sufficient to impair glucose-stimulated insulin release.