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The effect of short-term dietary supplementation with glucose on gastric emptying of glucose and fructose and oral glucose tolerance in normal subjects

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Summary

Recent observations indicate that gastric emptying may be influenced by patterns of previous nutrient intake. The aims of this study were to determine the effects of a high glucose diet on gastric emptying of glucose and fructose, and the impact of any changes in gastric emptying on plasma concentrations of glucose, insulin and gastric inhibitory polypeptide in response to glucose and fructose loads. Gastric emptying of glucose and fructose (both 75 g dissolved in 350 ml water) were measured in seven normal volunteers on separate days while each was on a ‘standard’ diet and an identical diet supplemented with 440 g/day of glucose for 4–7 days. Venous blood samples for measurement of plasma glucose, insulin and gastric inhibitory polypeptide levels were taken immediately before and for 180 min after ingestion of glucose and fructose loads. Dietary glucose supplementation accelerated gastric emptying of glucose (50% emptying time 82±8 vs 106±10 min, p=0.004) and fructose (73±9 vs 106±9 min, p=0.001). After ingestion of glucose, plasma concentrations of insulin (p<0.05) and gastric inhibitory polypeptide (p<0.05) were higher during the glucose-supplemented diet. In contrast, plasma glucose concentrations at 60 min and 75 min were lower (p<0.05) on the glucose-supplemented diet. We conclude that short-term supplementation of the diet with glucose accelerates gastric emptying of glucose and fructose, presumably as a result of reduced feedback inhibition of gastric emptying from small intestinal luminal receptors. More rapid gastric emptying of glucose has a significant impact on glucose tolerance.

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Abbreviations

GIP:

Gastric inhibitory polypeptide

T50:

50% gastric emptying time

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Horowitz, M., Cunningham, K.M., Wishart, J.M. et al. The effect of short-term dietary supplementation with glucose on gastric emptying of glucose and fructose and oral glucose tolerance in normal subjects. Diabetologia 39, 481–486 (1996). https://doi.org/10.1007/BF00400681

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  • DOI: https://doi.org/10.1007/BF00400681

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