Host vitamin D status is dependent on the microbiota. (MUC9P.747)

Abstract

Abstract Vitamin D deficiency is linked to susceptibility to inflammatory bowel disease (IBD). Mice deficient in vitamin D are more susceptible to experimental colitis than supplemented mice. Vitamin D alters the microbiota suggesting some of the effects of vitamin D on IBD are due to changes in the microbiota. Here we explored how the microbiota affect vitamin D metabolism using germ-free (GF) mice. Vitamin D is converted to 25D3. 25D3 is converted primarily in the kidney to 1,25D3, by 1α-OHase (Cyp27B1), or to 24,25D3 for degradation. Expression of Cyp27B1 was significantly higher in conventional (CV) versus GF kidneys. GF mice were given vehicle or 5μg vitamin D3 for 14 days and then conventionalized while maintaining their respective treatments for another 14 days. Liquid chromatography mass spectrometry was used to measure plasma vitamin D3, 25D3, 24,25D3, and 1,25D3 from GF mice before and after conventionalization. Vitamin D supplementation was less effective in GF mice. Conventionalized mice absorbed more vitamin D and had higher 25D3, 1,25D3, and 24,25D3. Furthermore, after correcting for differences in absorption between GF and CV mice, 1,25D3 was still significantly decreased in GF mice. This indicates GF mice neither absorb nor metabolize vitamin D normally. Differences in vitamin D metabolism between GF and CV mice suggest the microbiota play a role in regulating host vitamin D status, which could affect host immune responses and susceptibility to diseases like IBD.