1,25-Dihydroxycholecalciferol stimulates renal phosphate transport by directly altering membrane phosphatidylcholine composition.

Controversy exists regarding the mechanisms by which 1,25-dihydroxycholecalciferol (1,25(OH2)D3) alters membrane lipid composition and ion transport. Recent studies have demonstrated stimulation of the transfer of 1-acyl-2-(N-4-nitrobenz-2-oxa-1,3-diazole)aminocaproylphosphatidylcholine (NBD-PC) by 1,25(OH)2D3. In the present studies, brush border membrane vesicle phosphatidylcholine content was increased after incubation with liposomes composed of dioleoylphosphatidylcholine or beta-linoleyl, gamma-palmitoyl phosphatidylcholine and 1,25(OH)2D3 (10(-7) M). Vesicular phosphatidylcholine content was increased from control levels of 49.5 micrograms/mg protein to 56.9 and 58.5, respectively, after treatment with the liposomes containing 1,25(OH)2D3, P less than 0.05. When the vesicles were incubated with liposomes composed of beta-linoleyl, gamma-palmitoyl phosphatidylcholine, phosphate transport was stimulated from 231 +/- 20 to 431 +/- 41 pmol/mg protein per 15 s in the presence of 1,25(OH)2D3 if the vesicles were derived from vitamin D deficient rats and from 443 +/- 33 to 601 +/- 42 pmol/mg protein per 15 s if the vesicles were prepared from normal rats. Despite phosphatidylcholine transfer, incubation with liposomes composed of dioleoylphosphatidylcholine and 1,25(OH)2D3 did not stimulate phosphate transport. Furthermore, incubation of vesicles with liposomes and 1,25(OH)2D3 did not alter glucose transport.