LAUSR

Lower maternal vitamin D status during lactation is a common health problem. The objectives of this study were to investigate the effects of maternal 25-hydroxycholecalciferol (25-OH-D3) supplementation during lactation on maternal and neonatal bone health in a sow model. 32 Large White × Landrace sows were assigned randomly to one of two diets supplemented with 2000 IU/kg vitamin D3 (ND) or 50 μg/kg 25-OH-D3 (25-D). The experiment began on day 107 of gestation and continued until weaning on day 21 of lactation. Maternal 25-OH-D3 supplementation significantly decreased milk n-6:n-3 PUFA ratio, which supported bone formation of piglets. Supplementation with 25-OH-D3 altered bone turnover rate of sows and piglets, as evidenced by higher bone-specific alkaline phosphatase (BALP) concentration in serum. 25-D sows had significantly higher bone density and mechanical properties of tibias and femurs than ND sows. Calcium (Ca) absorption rate was higher in 25-D sows than ND sows, which was caused partially by the increased mRNA expressions of renal 1α-hydroxylase (CYP27B1) and duodenal vitamin D receptor (VDR), transient receptor potential vanilloid 6 (TRPV6), and calcium-binding protein D9k (CaBP-D9k). Maternal 25-OH-D3 supplementation increased tibial and femoral Ca content by up-regulating Ca-related gene expression in kidney (CYP27B1), ileum (VDR and claudin-2), and colon (VDR and CaBP-D9k), thus, activating 1,25-dihydroxyvitamin D3 [1,25-(OH)2-D3]-dependent Ca transport in piglets. In conclusion, improved milk fatty acids and higher mRNA expressions of calcitropic genes triggered by maternal 25-OH-D3 supplementation would be the potential mechanism underlying the positive effects of 25-OH-D3 on maternal and neonatal bone health.