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Low vitamin D status throughout life results in an inflammatory prone status but does not alter bone mineral or strength in healthy 3‐month‐old CD ‐1 male mice
Author(s) -
Jahani Raha,
Fielding Kristina A.,
Chen Jianmin,
Villa Christopher R.,
Castelli Laura M.,
Ward Wendy E.,
Comelli Elena M.
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201300928
Subject(s) - vitamin d and neurology , weaning , endocrinology , medicine , calcitriol receptor , offspring , vitamin , bone mineral , lactation , biology , physiology , osteoporosis , pregnancy , genetics
Scope The aim of this study was to assess if exposure to different levels of dietary vitamin D pre‐ and postweaning impacts the intestinal‐bone axis. Methods and results Female CD1 mice were exposed to high (5000 IU vitamin D 3 /kg diet, H) or low (25 IU vitamin D 3 /kg diet, L) vitamin D diet (modified AIN‐93G) during pregnancy and lactation. At weaning (postnatal day 21), a subset of the male offspring was sacrificed and another subset was assigned to receive their dams’ respective diet (HH and LL) or the other diet (HL and LH) until sacrifice at 3 months of age. Lower level of vitamin D resulted in reduced vitamin D receptor and increased expression of pro‐inflammatory genes in the colon at 3 months, lower numbers of colonic Bacteroides/Prevotella at postnatal day 21 and higher serum LPS concentration at adulthood. There was a programming effect of vitamin D on LPS levels. Mineral content, density, and strength of femurs and vertebrae were not affected. Conclusion Our findings suggest that low vitamin D exposure results in an inflammatory‐prone status that may contribute to or be a risk factor for several diseases including inflammatory bowel disease, obesity, diabetes, and cardiovascular diseases.