Date of this Version
Published in final edited form as: Vet Clin North Am Food Anim Pract. 2019 July ; 35(2): 277–288. doi:10.1016/j.cvfa.2019.02.001.
HHS Public Access Author manuscript
The consequences of prenatal stress on lifelong metabolic function and health was first proposed by David Barker and Nicholas Hales with the publication of their Thrifty Phenotype Hypothesis in the early 1990s.1,2 Subsequent studies in humans and animals have further demonstrated that stress-induced adaptive fetal programming leads to tissue-specific changes in metabolic function and growth capacity.3,4 Developmental adaptations to the intrauterine nutrient restriction that accompanies most maternofetal stressors target regulatory pathways for nutrient utilization in non-essential tissues such as skeletal muscle.4-6 This aids intrauterine survival by re-appropriating nutrients to support neural, cardiac, and endocrine tissue function but reduces metabolic efficiency and growth capacity in offspring. Stress-induced fetal adaptations are typically characterized by intrauterine growth restriction (IUGR) during late gestation and low birthweight.7,8 Poor postnatal growth and metabolic inefficiency associated with low birthweight can reduce value in livestock.4,8 Experimental models of IUGR livestock show how maternofetal stress from environmental, nutritional, or health conditions lead to fetal metabolic adaptations,5,9,10 but few studies have followed IUGR-born livestock after birth. Even less is known about how adaptive changes alter nutrient utilization in these offspring. In this review, we summarize the current literature that assesses nutrient partitioning in IUGR-born animals. In addition, we describe the key adaptive mechanisms underlying developmental changes that reduced muscle growth and impair metabolism.