Poor maternal nutrition during gestation alters the expression of genes involved in muscle development and metabolism in lambs.

Poor maternal nutrition during gestation can result in reduced muscle mass and increased adiposity of the muscle tissue in the offspring. This can have long-lasting consequences on offspring health and productivity. However, the mechanisms by which poor maternal nutrition affects postnatal muscle development are poorly understood. We hypothesized that poor maternal nutrition during gestation would alter expression of key pathways and genes involved in growth, development, and maintenance of the muscle of lambs. For this study, beginning at d 31 ± 1.3 of gestation, ewes were fed 100 (control), 60 (restricted), or 140% (overfed) of the NRC requirements. Within 24 h of birth, lambs were necropsied and semitendinosus muscle tissue was collected for gene expression analysis. Using RNA sequencing (RNA-seq) across dietary treatment groups, 35 and 10 differentially expressed genes were identified using the and reference annotations, respectively. Maternal overfeeding caused changes in the expression of genes involved in regulating muscle protein synthesis and growth as well as metabolism. Alternately, maternal nutrient restriction affected genes that are involved in muscle cell proliferation and signal transduction. That is, despite a similar phenotype, the genes identified differed between offspring born to restricted- or overfed, ewes indicating that the mechanism for the phenotypic changes in muscle are due to different mechanisms.

The effects of poor maternal nutrition during gestation on postnatal growth and development of lambs.

Poor maternal nutrition can affect the growth and development of offspring, which may lead to negative consequences in adult life. We hypothesized that lambs born to poorly nourished ewes would have reduced growth rate and increased fat deposition, with corresponding changes in the somatotropic axis, and leptin, insulin and glucose concentrations. Ewes ( = 36; 12/treatment) were assigned 1 of 3 diets; 100% (CON), 60% (RES), or 140% (OVER) of NRC requirements for TDN at d 31 of gestation until parturition. One lamb per ewe ( = 35; 11 to 12 per treatment) was used; 18 lambs were euthanized at d 1, and 17 were fed the same diet for 3 mo and then euthanized. Lamb crown rump length (CRL), heart girth, BW, and BCS were measured, and blood samples were collected at d 1 and then at weekly intervals until euthanasia. Averaged from d 1 until 3 mo, lambs from OVER ewes were larger compared with lambs born to CON ewes (BW [16.97 vs. 15.44 kg ± 0.60; = 0.09], ADG [0.23 vs. 0.21 ± 0.01 kg/d; = 0.01], and CRL [68.9 vs. 66.1 ± 0.80 cm; = 0.02]). On a BW basis, heart weight from lambs from RES (0.18 kg ± 0.03; = 0.03) ewes was greater than that of CON lambs (0.15 kg ± 0.03). Backfat thickness was reduced in RES lambs (0.11 ± 0.06; ≤ 0.04) compared with CON (0.20 ± 0.06) and OVER (0.26 ± 0.06) lambs. Concentrations of IGF-I at 3 mo and IGFBP-3 from weaning (d 56 of age) to 3 mo of age tended to be greater ( ≤ 0.06) in OVER lambs (334 ± 66 ng/mL and 175 ± 11 arbitrary units [AU], respectively) than CON lambs (149 ± 66 ng/mL and 140 ± 11 AU, respectively). At 3 mo, leptin was greater in OVER lambs compared with RES lambs (1.24 vs. 0.78 ± 0.13 ng/mL; < 0.05). Over time, average insulin concentrations were greater in OVER and RES lambs than CON lambs (0.49 and 0.49 vs. 0.33 ± 0.05 ng/mL; ≤ 0.02). However, concentrations of GH, IGFBP-2, glucose, triglycerides, and total cholesterol were not different ( > 0.10) between treatment groups. During in vivo glucose tolerance test, baseline insulin concentrations were 68% and 85% greater ( 0.01), respectively, in RES and OVER lambs compared with CON lambs. Similarly, the glucose:insulin ratio was greater in RES and OVER lambs compared with CON lambs ( 0.01). Thus, in this experiment, poor maternal nutrition during gestation influenced body size, organ growth, fat accumulation, and concentrations of IGF-I, IGFBP-3, leptin, and insulin of offspring during the first 3 mo of age.