Preweaning performance in intrauterine growth-restricted piglets: Characteristics and interventions

Intrauterine growth restriction (IUGR) is frequently observed in pig production, especially when using highly prolific sows. IUGR piglets are born with low body weight and shape indicative of differences in organ growth. Insufficient uteroplacental nutrient transfer to the fetuses is the leading cause of growth restriction in the pig. Supplementing the sow's gestation diet with arginine and/or glutamine improves placenta growth and functionality and consequently is able to reduce IUGR incidence. IUGR piglets are at higher risk of dying preweaning and face higher morbidity than their normal-weight littermates. A high level of surveillance during farrowing and individual nutrient supplementation can reduce the mortality rates. Still, these do not reverse the long-term consequences of IUGR, which are induced by persistent structural deficits in different organs. Dietary interventions peri-weaning can optimize performance but these are less effective in combating the metabolic changes that occurred in IUGR, which affect reproductive performance later in life. IUGR piglets share many similarities with IUGR infants, such as a poorer outcome of males. Using the IUGR piglet as an animal model to further explore the structural and molecular basis of the long-term consequences of IUGR and the potential sex bias could aid in fully understanding the impact of prenatal undernutrition and finding solutions for both species and sexes.

Automated summary

Intrauterine growth restriction (IUGR) is commonly observed in pig production, resulting in differences in organ growth. Insufficient uteroplacental nutrient transfer is the main cause of IUGR. Supplementing arginine and glutamine in the sow's diet improves placenta growth and reduces IUGR incidence. IUGR piglets have higher mortality rates and morbidity. Surveillance during farrowing and individual nutrient supplementation can reduce mortality rates. However, long-term consequences of IUGR, including persistent structural deficits in organs, cannot be reversed.