Bile acid uptake and calcium flux in brush border membrane vesicles.
Our laboratory has recently reported that intestinal bile acid malabsorption in cystic fibrosis (CF) is a primary mucosal cell defect. Others have suggested that elevated intracellular Ca++ levels in other cell types in CF may represent a common primary dysfunction in Ca++ efflux in these cells. We examined the possibility that intestinal bile acid absorption and Ca++ efflux in mucosal cells may be linked physiologically. Brush border membrane vesicles (BBMV) prepared from guinea pig ileum served as the experimental model to test this hypothesis. Ca++ (2.5 x 10(-3)M) present in the incubation medium did not alter the uptake of taurocholic acid (TCA) by BBMV. Also, TCA uptake into BBMV preloaded with Ca++ was not significantly different from that in BBMV not previously loaded with Ca++. Furthermore, with TCA present in the incubation medium, Ca++ efflux from preloaded BBMV was not altered. These data suggest that ileal TCA uptake, as measured by BBMV, is not dependent upon either intra- or extravesicular Ca++. Also, Ca++ efflux from BBMV is unaffected by TCA uptake. Although separate lines of evidence suggest that intestinal bile acid malabsorption and reduced plasma membrane Ca++ flux are primary defects in CF, we conclude that in the normal intestine these functions are independent physiological processes.
D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D006168:Guinea Pigs; D007082:Ileum / Q000378:metabolism / Q000648:ultrastructure*; D007413:Intestinal Mucosa / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D008871:Microvilli / Q000378:metabolism; D013656:Taurocholic Acid / Q000378:metabolism
D001647:Bile Acids and Salts; D013656:Taurocholic Acid; D002118:Calcium