Liponomic control of Ca2+ transport: relationship to mechanism of action of 1,25-dihydroxyvitamin D3.

Isolated vesicles prepared from the brush border membranes of chicken duodenal mucosal cells (enterocytes) take up calcium by a passive but saturable process. The rate of uptake (Vmax) is increased 2.5- to 3-fold, with no change in Km, in vesicles prepared from 1,25-dihydroxyvitamin D3 1,25(OH)2D3]-treated chickens compared to vesicles from vitamin D-deficient controls. Preincubation of vesicles with either cis- or trans-vaccinic acid (cVA or tVA, respectively) or their methyl esters in vitro also alters the rates of calcium transport. Methyl cVA causes an increase in rate of calcium uptake into vesicles from vitamin D-deficient chickens but not in those from 1,25(OH)2D3-treated chickens. This increase is 80-90% of that seen after 1,25(OH)2D3 treatment. Higher concentrations of methyl cVA produce no further increases. Conversely, methyl tVA causes a decrease in rate of calcium uptake in vesicles from 1,25(OH)2D3-treated chickens but no change in vesicles from vitamin D-deficient controls. This decrease reduces the rate of calcium uptake to nearly the same value as seen in vesicles from vitamin D-deficient controls. Higher concentration of methyl tVA produce no further suppression of uptake rate. The changes seen were in the Vmax and not in the Km of the transport process. The fatty acids did not alter the process of Na+-dependent glucose uptake in the same membrane. These data demonstrate that a small alteration in the lipid structure of this membrane can specifically shift the activity of the calcium transport process.