Abstract
Poor maternal nutrition during gestation alters offspring muscle composition, fiber number, and postnatal growth. Additionally, poor maternal nutrition impacts offspring whole body and stem cell metabolism. We hypothesized that over- or restricted-feeding ewes during gestation would alter the offspring longissimus muscle metabolome. Pregnant Western White-faced ewes (n = 47) were individually fed 60% (restricted), 100% (control), or 140% (over) of NRC requirements for TDN starting at d 30.2 ± 0.2 of gestation. At days 90 and 135 of gestation, ewes were euthanized for fetal muscle collection. Another group of ewes were allowed to lamb and offspring were necropsied within 24 h of birth. Mass spectrophotometry of longissimus muscle samples (n = 8 fetuses per treatment per time point) identified 612 metabolites. Data were analyzed by ANOVA for main effects of treatment, time point, and their interaction. Compared with controls, maternal over-feeding altered metabolites in 63 pathways and maternal restricted-feeding altered metabolites in 56 pathways (P < 0.05). Maternal over-feeding decreased concentrations of 1 phosphatidylcholine (PC) metabolite at d 90, 2 PC metabolites at d 135, and 4 PC metabolites at birth compared with controls (P < 0.05). Additionally, at d 135, maternal overfeeding increased 1 phosphatidylethanolamine (PE) metabolite while reducing 10 PE metabolites at birth compared with controls (P < 0.05). Offspring from overfed ewes had decreased concentrations of 12 lysolipids at birth compared with controls (P < 0.05). Maternal restricted-feeding increased expression of reduced glutathione 3.07-fold at d 90 (P = 0.008), whereas at d 135, oxidized glutathione was decreased 0.21-fold compared with control (P = 0.03). Thus, maternal over-feeding may promote increased lipid oxidation in offspring muscle, which may predispose offspring to altered lipid utilization and storage postnatally. Maternal restricted-feeding resulted in alterations in glutathione metabolism, potentially indicative of changes to redox status in these offspring.