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Effect of protein-calorie malnutrition on intestinal disaccharidase activities and disaccharide absorption in the rat Wilson, Judith Leslie

Abstract

The purpose of the present investigation was to study the effect of prolonged protein-calorie malnutrition on intestinal disaccharidase activities and on disaccharide absorption, as carbohydrate intolerance is a major problem in children suffering from protein-calorie malnutrition. Four groups of rats (90 to 120 grams) were fed the following diets for 8 to 9 weeks: control (18% lactalbumin, 66% carbohydrate); low protein low carbohydrate (0.5% lactalbumin, 66% carbohydrate); low protein high carbohydrate (0.5% lactalbumin, 83.5% carbohydrate); and low protein restricted (1% lactalbumin, restricted to 4 grams per day). After 8.5 weeks, part of the group on the 0.5% lactalbumin low carbohydrate diet was fed the control diet (18% lactalbumin, 66% carbohydrate) for 8 weeks. At the end of the feeding period, the following assays were performed: 1) in vivo absorption of radioactive (¹⁴C) lactose, sucrose, and maltose; 2) activities of intestinal lactase, sucrase, and maltase; 3) plasma albumin concentrations; and 4) mucosal protein concentrations. In the three protein deficient groups (0.5% lactalbumin low carbohydrate, 0.5% lactalbumin high carbohydrate, and 1% lactalbumin), the activity of both the jejunal and ileal disaccharidases and the absorption of lactose, sucrose and maltose were significantly higher when compared with the controls. The jejunal sucrase and maltase activities were significantly higher in the 0.5% lactalbumin high carbohydrate group than in the 0.5% lactalbumin low carbohydrate group, but the absorption of lactose, sucrose and maltose were alike. When the 1% lactalbumin (restricted to 4 grams per day) and the 0.5% lactalbumin low carbohydrate groups were compared, there were no statistically significant differences in the specific activities of the intestinal disaccharidases or the absorption of the disaccharides. The absorption of lactose, sucrose, or maltose were similar in the controls and the protein repleted group. The disaccharidase activities were also similar in these two groups except for a significant depression of jejunal maltase and ileal sucrase and maltase activities in the protein repleted group. Therefore, these results indicate that protein deprivation in rats for 8.5 weeks causes an increase in specific activities of the intestinal disaccharidases in both the jejunum and ileum, and that these changes caused by protein depletion may be reversed by feeding a diet high in protein. Also, an increase in the carbohydrate content of the protein deficient diet results in an induction of jejunal sucrase and maltase activities. The high specific activity of the intestinal disaccharidases following protein-calorie malnutrition may be in part due to a preferential loss of structural proteins rather than to an increase in enzymatic protein in the intestinal mucosa. The increase in the disaccharidase activities in the protein deficient rats is accompanied by an increase in disaccharide absorption which could be due to the higher levels of disaccharidases or to an increase in the transport of the constituent monosaccharides. The demonstration of statistically significant differences in sucrase and maltase activities between the 0.5% lactalbumin high carbohydrate and the 0.5% lactalbumin low carbohydrate groups without a concomitant increase in sucrose and maltose absorption, supports the view that the higher absorption of sucrose and maltose in the protein deficient rats is a result of increased monosaccharide transport. The results of this study are not consistent with the suggestion that protein-calorie malnutrition is responsible for disaccharide intolerance in children.

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