ISSN:
1432-5233
Schlagwort(e):
Key words High sucrose diet
;
Glucose tolerance
;
Islet function
;
Insulin release
Quelle:
Springer Online Journal Archives 1860-2000
Thema:
Medizin
Notizen:
Abstract 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.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1007/BF02048545
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