PHYSIOLOGY AND ENDOCRINOLOGY SYMPOSIUM: Postnatal reproductive development and the lactocrine hypothesis.

Abstract

Maternal effects on development can program cell fate and dictate offspring phenotype. Such effects do not end at birth, but extend into postnatal life through signals communicated from mother to offspring in first milk (colostrum). Transmission of bioactive factors from mother to offspring as a specific consequence of nursing defines a lactocrine mechanism. The female reproductive tract is not fully formed at birth (postnatal day = PND 0). Data for ungulates and mice indicate that disruption of development during neonatal life can have lasting effects on the form and function of uterine tissues. Uterine growth and histogenesis proceed in an ovary-independent manner shortly after birth, suggesting that extra-ovarian inputs are important in this process. Data for the pig indicate that lactocrine signals communicated within 12 to 48 h from birth constitute one source of such uterotrophic support. Disruption of lactocrine signaling, either naturally, by limited colostrum consumption, or experimentally, by milk replacer feeding, alters neonatal porcine uterine development and can have negative consequences for reproductive performance in adults. Substantial differences in endometrial and uterine gene expression between colostrum- and replacer-fed gilts were evident by PND 2, when RNA sequencing revealed over 800 differentially expressed, lactocrine-sensitive genes. Lactocrine-sensitive biological processes identified through transcriptomic studies and integrated microRNA-mRNA pathway analyses included those associated with both cell-cell and ESR1 signaling, and tissue development. Evidence for the pig indicates that colostrum consumption and lactocrine signaling are required to establish a normal uterine developmental program and optimal uterine developmental trajectory.