Postnatal Nutrient Repartitioning due to Adaptive Developmental Programming

Abstract

Fetal stress induces developmental adaptations that result in intrauterine growth restriction (IUGR) and low birthweight. These adaptations reappropriate nutrients to the most essential tissues, which benefits fetal survival. The same adaptations are detrimental to growth efficiency and carcass value in livestock, however, because muscle is disproportionally targeted. IUGR adipocytes, liver tissues, and pancreatic β-cells also exhibit functional adaptations. Identifying mechanisms underlying adaptive changes is fundamental to improving outcomes and value in low birthweight livestock. The article outlines studies that have begun to identify stress-induced fetal adaptations affecting growth, metabolism, and differential nutrient utilization in IUGR-born animals.

Keywords: Developmental origins of health and disease; Fetal adaptations; Fetal stress; Nutrient repartitioning; Thrifty phenotype.

Figure 1.

Stress-induced fetal adaptations cause low birthweight livestock to re-appropriate dietary nutrients. Less nutrients are utilized for skeletal muscle growth and more are redirected to visceral fat deposits and, to a lesser extent, intramuscular and subcutaneous fat deposits.

Figure 2.

Stress induced fetal adaptations impair tissue responsiveness to insulin. In prenatal and early postnatal stages, impaired insulin action is masked by transient increases in insulin sensitivity, which benefits IUGR fetal survival.