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125 30 30 8 8 M. Kergoat D. Bailbe B. Portha Laboratory of Development Physiology University of Paris Paris France Summary The effects of chronic high sucrose feeding for 1 month on in vivo and in vitro insulin secretion and on in vivo insulin action were studied in rats with non-insulin-dependent diabetes. As compared to the standard diet, the high sucrose diet induced an increase of the in vivo insulin response to an intravenous load and deteriorated the glucose tolerance as attested by significantly lower rates of glucose disppearance (K values, p <0.001). The increased insulin secretion in response to glucose in vivo seems to be related to a slight increase of the pancreatic B-cell reactivity to glucose, since it was still observed in vitro with the isolated perfused pancreas preparation. By contrast, B cells of sucrose-fed rats exhibited in vitro a significantly lowered ( p <0.01) response to acetylcholine and arginine. The insulin action in the sucrose-fed diabetic rats was quantified in vivo with the insulin-glucose clamp technique. The effects of different concentrations of insulin on glucose production and glucose utilisation were studied in anaesthetized rats while in the postabsorptive state. The basal glucose utilisation was found significantly higher ( p <0.001) in sucrose-fed rats. During the clamp studies the glucose utilisation induced by submaximal (450 mU/l) insulin level was significantly less important ( p <0.01) in the sucrose-fed rats than in the chow-fed rats. Following a maximal hyperinsulinaemia (5000 mU/l) the glucose utilisation was similar in both groups. This suggests that insulin-mediated glucose uptake is decreased over the range of submaximal plasma insulin levels in the sucrose-fed diabetic rats. In the basal state hepatic glucose production was significantly higher ( p <0.001) in sucrose-fed rats. During the clamp studies, the suppression of glucose production induced by submaximal or maximal insulin levels was significantly less effective ( p <0.01) in the sucrose-fed rats as compared to chow-fed rats, thus suggesting that the liver becomes resistant to insulin action after sucrose feeding. Finally, these results suggest that restriction of complex carbohydrates in favor of sucrose in insulin-deficient rats leads to metabolic events likely to develop insulin resistance in target tissues.
Diabetologia – Springer Journals
Published: Aug 1, 1987
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