Intake of ergosterol increases the vitamin D concentrations in serum and liver of mice

Factors that can modify the bioavailability of orally administered vitamin D are not yet widely known. Ergosterol is a common fungal sterol found in food which has a chemical structure comparable to that of vitamin D. This study aimed to investigate the effect of ergosterol on vitamin D metabolism. Therefore, 36 male wild type-mice were randomly subdivided into three groups (n = 12) and received a diet containing 25 mu g vitamin D-3 and either 0 mg (control), 2 mg or 7 mg ergosterol per kg diet for 6 weeks. To elucidate the impact of ergosterol on hepatic hydroxylation of vitamin D-3 human hepatoma cells (HepG2) were treated with different concentrations of ergosterol. Concentrations of vitamin D-3 and 25-hydroxyvitamin D-3 (25(OH)D-3) in cells, livers and kidneys of mice and additionally 24,25-dihydroxyvitamin D-3 (24,25(OH)(2)D-3) in serum were quantified by LC-MS/MS. The concentration of 1,25-dihydroxyvitamin D-3 (1,25(OH)(2)D-3) in serum was analyzed by commercially-available enzyme immuno assay. The concentrations of cholesterol and triglycerides were analyzed in livers of mice by photometric assays. Analyses revealed that mice receiving 7 mg/kg ergosterol with their diet had 1.3-, 1.7- and 1.5-times higher concentrations of vitamin D-3 in serum, liver and kidney, respectively, than control mice (P < 0.05), whereas no significant effects were observed in mice fed 2 mg/kg ergosterol. The hydroxylation of vitamin D remained unaffected by dietary ergosterol, since the concentration of 25-hydroxyvitamin D-3 in serum and tissues and the concentrations of 1,25(OH)(2)D-3 and 24,25(OH)(2)D-3 in serum were not different between the three groups of mice. The lipid concentrations in liver were also not affected by dietary ergosterol. Data from the cell culture studies showed that ergosterol did not influence the conversion of vitamin D-3 to 25(OH)D-3. To conclude, ergosterol appears to be a modulator of vitamin D-3 concentrations in the body of mice, without modulating the hydroxylation of vitamin D-3 in liver.