Submitted to: Society for the Study of Reproduction Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 3/6/2016
Publication Date: 7/16/2016
Citation: Vallet, J., Miles, J., Freking, B., Meyer, S. 2016. Glucosamine supplementation affects placental development in swine [abstract]. Society for the Study of Reproduction Annual Meeting. Abstract # 287 (Scientific Program p. 181). Available: http://www.ssr.org/sites/ssr.org/files/uploads/attachments/node/320/2016_ssr_abstracts.pdf
Technical Abstract: Previous studies indicated that the depth of the folds of the endometrial epithelial-fetal trophoblast bilayer of the pig placenta is increased in the placenta of small fetuses during late gestation, and that hyaluronan metabolism plays a role in the process. Given this, we hypothesized that glucosamine supplementation would support fold development by providing substrate for hyaluronan synthesis in the placenta. In experiment 1, gilts were unilaterally hysterectomized-ovariectomized (UHO), mated at estrus, and received either glucosamine (n = 16) or glucose (n = 17) supplementation (10 g) as a top dress on their daily feed from day 85 to day 105 of gestation, when they were slaughtered and the reproductive tract was collected. Blood samples were collected from each living fetus and each living (beating heart) fetus was counted and weighed. Uterine wall samples were collected from placentas corresponding to the largest and smallest fetus in each litter for histological evaluation of fold development. Placental tissues were also collected to evaluate hyaluronan content, and fetal blood samples were measured for glucose and fructose concentrations. Glucosamine supplementation tended (P = 0.098) to increase the number of live fetuses compared to glucose (8.4 ± 0.6 versus 6.9 ± 0.6, respectively). Glucosamine significantly increased the depth of folds compared to glucose, regardless of fetal size (798 ± 26 versus 723 ± 25 microns, respectively). Fetal blood glucose and fructose concentrations were affected by fetal and placental weights, and glucosamine supplementation appeared to stabilize these differences compared to glucose supplementation. There was no effect of supplementation on placental hyaluronan content. In a second experiment, glucosamine (n = 128) or glucose (n = 127) supplementation was provided to mated sows (parity 2 to 8) from day 85 to farrowing in a commercial setting. At birth, total born, live born, stillborn and mummies were counted. Total born (15.6 ± 0.4 versus 15.2 ± 0.4) and live born (14.0 ± 0.3 versus 13.8 ± 0.3) did not differ between glucosamine and glucose treated sows. There was a treatment by parity interaction (P < 0.05) for stillborn pigs. Glucosamine treatment increased the number of stillborn piglets in late parity (7 and 8) by approximately 1 piglet compared glucose. This differed from other parities, in which treatment did not affect stillbirth rate. We conclude that glucosamine supplementation increased the depth of folds and tended to increase uterine capacity in gilts, but the dose used did not affect litter size in sows in a commercial setting. It is possible that the increase in stillborn piglets in later parity sows in experiment 2 was due to effects of glucosamine supplementation on the thickness of the placenta, which has been suggested to influence stillbirth rate.