211 Overcoming the Growth Deficits Programmed by Maternofetal Stress

Abstract Prolonged maternofetal stress stunts placental development and causes fetal programming that reduces growth birthweight. Low birthweight due to intrauterine restriction (IUGR) of the fetus increases perinatal mortality. More commonly, however, it results in lifelong impairment muscle capacity metabolic function. In humans, low risk for obesity, diabetes, other disorders by an estimated 18-fold. Similarly, livestock exhibit greater early death loss, poor efficiency, lower-quality carcasses at harvest. These animals manifest feed-to-gain ratios, less lean mass, fat deposition. Together, these outcomes increase production costs, decrease value, reduce amount meat produced per animal. The mechanisms linking induced IUGR impaired postnatal efficiency are largely unknown. However, recent findings neonatal lambs experimentally maternal heat inflammation (and pair-fed controls) indicated skeletal muscle-centric adrenergic inflammatory pathways. Specifically, studies found reduced β2 tone enriched signaling changes coincided with intrinsic myoblast dysfunction, fiber hypertrophy, glucose metabolism. Additionally, exhibited β cell function may also be associated programming. Subsequent have investigated as potential therapeutic targets interventions treatments, which is a fundamental step developing strategies improve humans livestock.