Small Intestinal Membrane Vesicles Research Articles

Changes in glucose uptake by and phlorizin binding to brush-border membrane vesicles of small intestine from streptozotocin-induced diabetic rats.

The changes in the intestinal glucose transport in streptozotocin-induced diabetic rats have been demonstrated with brush-border membrane vesicles. When Na+-dependent D-glucose uptake and phlorizin binding activities were compared, both significantly increased either in the jejunum or ileum of diabetic rats compared with those of control. Kinetic studies showed the increases in the Vmax of glucose transport and the maximum binding of phlorizin (Bmax), whereas the Kt and Kd remained unchanged, respectively. These results suggested that the increase in glucose transport in diabetic rat intestine was due to the increase in the number of the intact glucose transporters.

84. THE EFFECTS OF VITAMIN E DEFICIENCY ON SMALL INTESTINAL TRANSPORT FUNCTION

The gastrointestinal mucosa is vulnerable to damage by lipid peroxidation. Vitamin E (E) is a powerful membrane bound antioxidant present in high concentration in enterocytes. We have studied the effects of E deficiency on mucosal function. 20 day old male Wistar rats were placed on a diet either deficient in E or one to which E (100mg/kg) had been added. Brush border membrane vesicles of small intestine were prepared by a Ca++ precipitation method and glucose and sodium uptake measured. Na+K+ATPase, cAMP and cGMP were determined in mucosal homogenates. Na+ stimulated glucose uptake was rapid with an ‘overshoot’ in both groups but after 9 months of E deficiency maximal glucose uptake was signifiqantly impaired (757±116 vs 1152±324 pmol/hr/mg protein; mean±1SD; n=5; p<0.05). H+ stimulated Na+ uptake was similarly reduced (380±148 vs 713±181, p<0.02). In the absence of a Na+ or H+ gradient, uptake of glucose and Na+ was not affected by E deficiency. No significant differences in Na+K+ATPase activity or cyclic nucleotide concentrations were observed. These data show that intestinal transport is disturbed in E deficiency and suggest that this is due to an effect on apical membrane transporters rather than on passive permeability or the enterocyte Na+ pump. We speculate that E deficiency may contribute to the malabsorption seen in some states of malnutrition.

Effects of pH and sodium on phosphate transport across brush border membrane vesicles of small intestine.

It is known that, in isolated intact rat small intestine, the phosphate (Pi) transport from lumen to tissue increases when the pH of the luminal solution is reduced1. A similar observation has also been reported in brush border membrane vesicles (BBMV) from rat small intestine2. These results have suggested that the increase in mono- respective to divalent phosphate, which occurs when pH is reduced, was responsible for the higher uptake found at acidic pH, thus leading to the conclusion that primary Pi was transported across the brush border of small intestinal epithelium. Such a conclusion, however, is valid only if direct effects of pH on the phosphate transport system are excluded.KeywordsBrush Border MembranePhosphate TransportPhosphate UptakeBrush Border Membrane VesicleRabbit Small IntestineThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.