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Title:   Author  item
                                            Vallet, Jeffitem
                                            McNeel, Anthonyitem
                                            CALDERON-DIAZ, JULIA - Iowa State Universityitem
                                            STALDER, KENNETH - Iowa State Universityitem
                                            PHILLIPS, C - Murphy Brown Llcitem
                                            Rohrer, Garyitem
                                            Miles, Jeremyitem
                                            Freking, Bradley

                                                         - *Brad*
  Submitted to: Society for the Study of Reproduction Annual Meeting
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 6/2/2015
                                    Publication  Date: 6/2/2015
                                    Citation: Vallet, J.L., McNeel, A.K., Calderon-Diaz, J.A., Stalder, K.J., Phillips, C.E., Rohrer, G.A., Miles, J.R., Freking, B.A. 2015. Can we make the pig placenta work better? [abstract]. Society for the Study of Reproduction Annual Meeting. pp. 40-41 (Abstract #107). Available: https://www.ssr.org/Interpretive Summary:
                                Technical Abstract: The number of piglets born alive at each parity contributes to the efficiency of swine production. Moreover, piglet birth weights affect both survival to weaning and future growth rate. Litter size and birth weight are influenced by placental function. The pig placenta is classified as diffuse epithelial-chorial because no erosion of fetal or maternal tissue occurs. Because of the superficial placentation, there is a tendency to think about the pig placenta as only that portion that originates from the fetus. However, pig placental function originates from components of both maternal (i.e., the uterus) and fetal (i.e., the “placenta”) origin. Uterine space is a primary determinant of placental function, which has been demonstrated by the relationship between conceptus survival and uterine length per conceptus. Although this relationship has been known for decades and uterine length is highly variable in pigs, little is known regarding the physiological mechanisms that control this trait. We performed a genomic analysis for uterine length in ~1,000 post-pubertal gilts from a commercial maternal line as part of a National Pork Board-funded study. Preliminary genomic analysis of these data revealed at least 5 quantitative trait loci for uterine length (ranges of effects of 30 to 67 cm in length). These loci may be exploited to increase uterine length, potentially improving placental size and function if the number of embryos is held constant. Further improvements in placental function require an understanding of how the placenta works. It is helpful to divide placental function into structural factors that contribute to nutrient transport generally and nutrient-specific factors that promote transport of individual nutrients or classes of nutrients. Structural factors include the microscopic architecture of the maternal-fetal interface in relationship to maternal and fetal blood flow. Previous results indicated that placental microarchitecture is altered in the placenta of small fetuses in ways that are consistent with improvement of nutrient transport but that these beneficial modifications may be limited by placental stromal tissue. From these results, we proposed the concept of feeding the placental stroma as a way to improve placental function. A primary component of placental stroma is hyaluronan, which is made up of glucuronic acid and glucosamine. Supplementation of diets of pregnant gilts with glucosamine in late gestation tended (P = 0.09) to improve litter size and resulted (P = 0.05) in beneficial changes in placental microarchitecture, suggesting that our concept may be correct. We have also performed a transcriptomic analysis of fetal placenta trophoblast cells using RNA-seq. This resulted in a comprehensive list of nutrient transporter genes along with their expression levels. The two most expressed sugar transporters (SLC2A genes) were SLC2A12 and 13, corresponding to GLUT12 and proton-coupled myoinositol transporter (HMIT). Immunohistochemical analysis for HMIT confirmed its presence within the maternal-fetal interface. This result suggests active transport of inositol by the pig placenta for reasons that are currently unclear. Nevertheless, inositol represents a potential further avenue to explore that could improve placental function and is an example of many possible interventions that might come from an improved understanding of specific nutrient transport mechanisms.


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