Effect of dietary carbohydrate on monosaccharide uptake by mouse small intestine in vitro.

Abstract

SUMMARY1. Using intestinal sleeves in vitro, we studied the effect of dietary carbohydrate on active monosaccharide uptake in mice.2. Dietary carbohydrate did not affect numerous parameters ofintestinal structure, such as length, circumference, weight, protein content, villus dimensions and density, and area at the villus level.3. Mice on a carbohydrate-free diet had active D-glucose uptake relatively independent of position along the small intestine. A carbohydrate-containing diet reversibly and within 1 day stimulated uptake except in the ileum, restoring the proximal-to-distal gradient in glucose uptake normally observed.4. This stimulation involved a 81-116 % increase in the Michaelis-Menton constant Vmax, and also an apparent increase in the Michaelis-Menton constant Km, that may however be an artifact arising from unstirred-layer effects.5. Active uptake of 3-0-methyl-D-glucose also increased, permeability to glucose remained unchanged, and proline uptake reversibly decreased (probably due to the lower protein content of the carbohydrate-containing diets).6. The effect of fasting on active monosaccharide uptake seemed largely due to withdrawal of dietary carbohydrate, rather than of calories per se.7. It is concluded that dietary carbohydrate causes induction of monosaccharide carriers in the intestine, along with its more familiar induction of pancreatic amylase and intestinal disaccharidases. Substrate-dependent carrier induction may be physiologically significant in maintaining the proximal-to-distal gradient of glucose transport.8. An appendix presents measurements of villus area as a function ofposition along the intestine.

Adaptive Changes of Sugar Absorption in Rat Small Intestine during Fasting and Refeeding

“…Furthermore, it is also important to consider the metabolism of epithelial cells. For example, it is known that the effect of fasting on active uptake of monosaccharides seems to be largely due to the withdrawal of dietary carbohydrate [24] and that glucose transport is induced by an increase in blood glucose in diabetic rat intestine [25]. In our study the changes in blood glucose paralleled the 4PD evoked by glucose during fasting and refeeding.…”

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

“…1 (Brown & Sepulveda, 1985), and chicken intestinal cells produced Jmax = 10 nmol min-' mg-' and Kt = 2-4 mm (Kimmich & Randles, 1984). In whole preparations of mouse small intestine, monosaccharide transport was also high (Diamond & Karasov, 1984 The isolated cells maintained a linear production of lactate from 5 mM-D-glucose in the uptake medium. Regression analysis of 0-15 min incubations yielded a lactate production rate of 38 nmol min-(mg cell protein)-1 (data not shown), in good agreement with data from rat intestinal cells (Watford, Lund & Krebs, 1979) and jejunal loop perfusions of rat (Kellett & Barker, 1989) and mouse (J.…”

Postprandial morphological response of the intestinal epithelium of the Burmese python (Python molurus)

“…Changes in diet composition, meal size, and meal frequency have all been demonstrated to induce alterations of the morphology and/or function of the intestinal epithelium. Examples of intestinal plasticity among mammals include the doubling of intestinal D-glucose uptake by mice switched from a low carbohydrate to a high carbohydrate diet, the 50% increase in intestinal mass of mice that have increased food intake during cold exposure and/or lactation, and the atrophy of the small intestine of ground squirrels during the long-term fast of hibernation and subsequent intestinal hypertrophy with feeding following spring emergence (Carey, 1990;Diamond and Karasov, 1984;Hammond et al, 1994).…”