Demonstration of the Disaccharide Effect in Nutritionally Stressed Rats

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Abstract
Male Wistar rats were either starved for 2 days and refed for 2 days or meal-fed (2 hours/day) for 2 or 6 weeks. Diets contained 45% carbohydrate as either disaccharides (maltose, sucrose) or the monosaccharide equivalents (glucose, invert sugar). Changes in the activities of glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme (ME) in the liver and epididymal adipose tissue, relative liver and epididymal fat pad sizes, fasting serum insulin levels, and food efficiencies were determined. The response to the diets containing the monosaccharide equivalents (glucose or invert sugar) was used as the basal response. With starvation-refeeding or 6 weeks of meal-feeding, the activities of G6PD and ME in the liver were greater with maltose than with glucose (disaccharide effect), but with sucrose only starvation-refeeding induced the effect. The disac-charide effect increased the activities of G6PD and ME in the liver and decreased the activities in the adipose tissue. Rats meal-fed the disaccharide diets for 2 weeks had greater fasting insulin levels and relative liver and epididymal fat pad sizes than did rats fed the equivalent monosaccharide diets. The disaccharide effect increased food efficiency significantly after both 2 and 6 weeks of meal-feeding. In rats starved and refed carbohydrates containing fructose, activities of G6PD and ME were higher in liver and lower in adipose tissue than in rats refed carbohydrates containing only glucose (fructose effect); with meal-feeding only the liver showed a fructose effect. These findings support the hypothesis that dietary disaccharides produce metabolic effects which are different in magnitude than those produced by their equivalent monosaccharides.