25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol: conversion impaired by systemic metabolic acidosis.
An acute systemic acidosis in vitamin D depleted rats that was induced by ammonium chlroide feeding resulted in defective biological hydroxylation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol. Impaired enzymatic hydroxylation occurred despite the presence of either hypophosphatemia or hypocalcemia. The data suggest that acidosis interfers with the adaptive enzymatic control of 25-hydroxycholecalciferol metabolism in the vitamin D depleted state.
D000138:Acidosis / Q000097:blood / Q000139:chemically induced / Q000378:metabolism*; D000643:Ammonium Chloride; D000818:Animals; D002118:Calcium / Q000097:blood; D004100:Dihydroxycholecalciferols / Q000096:biosynthesis; D006887:Hydroxycholecalciferols / Q000097:blood / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism; D008297:Male; D010758:Phosphorus / Q000097:blood; D051381:Rats
D004100:Dihydroxycholecalciferols; D006887:Hydroxycholecalciferols; D000643:Ammonium Chloride; D010758:Phosphorus; D002118:Calcium