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 β-inoleyl, γ-palmitoyl phosphatidylcholine and 1,25(OH)₂D₃ (10^-7 M). Vesicular phosphatidylcholine content was increased from control levels of 49.5 μg/mg protein to 56.9 and 58.5, respectively, after treatment with the liposomes containing 1,25(OH)₂D₃, P < 0.05. When the vesicles were incubated with liposomes composed of β-inoleyl, γ-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.