Insights into Nutrient Inputs that Affect the Initiation of Bone Lesions in Pigs

Abstract Text:

Understanding the etiology of nutrients involved in the initiation of bone lesions is hampered by the inability to reproduce lesions under controlled conditions. Characterization of lesions associated with an accidental omission of vitamin D (D) in sow diets within our research herd catapulted my research career and led to an ability to consistently reproduce hypovitaminosis D induced kyphosis in young pigs. Kyphosis was induced by feeding D deficient diets to sows during gestation and lactation and subsequent nursery diets deficient in D, with marginal deficiencies in Ca and P. Our experiments characterized the influence of D on gross and molecular changes during the initial stages of bone lesions. Evidence of maternal dietary D carryover effects on subsequent pig bone development have been an exciting outcome. Sow diets included 0 (-D), 325 (+D), and 1750 (++D) IU D₃/kg diet. Although not specifically designed to evaluate effects of D on reproduction, no effects of dietary D were detected on live, still, and total birth numbers. At weaning pigs were fed diets with 0 (-D) or 280 (+D) IU D₃/kg and relatively minor modifications to dietary Ca and P to exasperate responses to dietary D.  Only minor responses to maternal diets were detected in pig growth and bone mineral content (BMC) at birth and 3 wk. However at 8 wk pigs produced by –D sows had an 11% reduction in growth and a 25% reduction in BMC regardless of nursery diet. A significant interaction between maternal and nursery diets was also detected.  Pigs fed –D, high P diets responded differently if produced by ++D sows. Significant maternal and nursery diet effects on mRNA expression of genes involved in D homeostasis (25-hydroxylase and 1α-hydroxylase) and bone metabolism (fibroblast growth factor 23 and osteocalcin) were also evident in pig tissues. Specific genes of interest are matrix metalloproteinases 9 and 13 and vascular endothelial growth factor as these D mediated genes may identify specific alterations that lead to the initiation of bone lesions. Our results with the hypovitaminosis D kyphotic pig model has illustrated the importance of maternal diets on neonatal skeletal development. However, the design of our studies have not allowed discernment between gestation and lactation effects. Continued studies with this model will lead to a more complete understanding of the etiology of nutrient factors involved in the initiation of bone lesions, which apparently occur during fetal development.

Keywords:

Vitamin D; Kyphosis; Maternal carryover