Supplemental silicon increases plasma and milk silicon concentrations in horses.

The primary objective of this research was to determine the effect of supplemental dietary silicon (Si) on plasma and milk Si concentrations of lactating mares and the subsequent effect on plasma Si concentrations in nursing foals. Additionally, the role of Si on altering biochemical markers of bone turnover was investigated, because supplemental Si may be advantageous in enhancing bone health. Twelve Arabian mare/foal units were pair-matched by foaling date and randomly assigned to two groups, Si-supplemented (Supplemented) or control (Control). Blood and milk samples were taken on d 0, 15, 30, and 45, d 0 being the 1st d after parturition. Plasma and milk (or colostrum) Si concentrations were determined and serum was analyzed for osteocalcin, carboxy-terminal pyridinoline cross-linked telopeptide region of type I collagen, and pyridinoline and deoxypyridinoline crosslinks. All Supplemented mares had higher (P < 0.01) plasma Si concentrations than Control by d 30, and Supplemented mares' milk had higher (P < 0.01) Si concentrations on d 45 than Control mares' milk. By d 45, foals of Supplemented mares had higher (P < 0.01) plasma Si concentrations than foals of Control mares. Supplemental Si did not influence (P > 0.36) bone metabolism in foals; however, trends (P < 0.10) for altered bone metabolism were observed in postpartum mares. Results indicate that supplemental Si increases plasma and milk Si concentrations. Further research is required to determine whether Si has a role in altering serum biochemical markers of bone and collagen activity.

The turkey transcription factor Pit-1/GHF-1 can activate the turkey prolactin and growth hormone gene promoters in vitro but is not detectable in lactotrophs in vivo.

The transcription factor Pit-1/GHF-1 plays an important role in regulating the prolactin (Prl) and growth hormone (GH) genes in mammals. In this study, the role that Pit-1 plays in regulating the prolactin and growth hormone genes in avian species was examined by cotransfection assays and immunofluorescence staining of pituitary sections. In cotransfection assays, turkey Pit-1 activated the turkey Prl, turkey GH, and rat Prl promoters 3.8-, 3.7-, and 12.5-fold, respectively. This activation was comparable to rat Pit-1 activation of these same promoters. A point mutation in the turkey Pit-1 cDNA, which changed leu-219 to ser-219, resulted in a 2-, 2-, and 10-fold reduction in the activation of the turkey Prl, turkey GH, and rat Prl promoters, respectively. Unexpectedly, coexpression of tPit-1 (leu-219) and tPit-1(ser-219) activated turkey Prl and rat Prl promoters 9.4- and 35.9-fold, respectively, but had no effect on the turkey GH promoter. Dual-label immunofluorescence analysis of turkey pituitary sections revealed that Pit-1 was not detectable in prolactin-staining cells but was detectable in GH-staining cells. Taken together, these data indicate that in the domestic turkey, Pit-1 can activate the turkey Prl promoter in vitro, but does not appear to play a role in regulating Prl gene expression in vivo. Pit-1, however, still likely plays a role in regulating GH gene expression.