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Poor maternal nutrition during gestation negatively affects offspring growth and metabolism. To evaluate the impact of maternal nutrient restriction and realimentation on metabolism in the fetal liver, skeletal muscle, and circulation, on day 50 of gestation, ewes (n = 48) pregnant with singletons were fed 100% (CON) or 60% (RES) of requirements until day 90 of gestation, when a subset of ewes (n = 7/treatment) were euthanized, and fetal samples were collected. The remaining ewes were maintained on a current diet (CON-CON, n = 6; RES-RES, n = 7) or switched to an alternative diet (CON-RES, RES-CON; n = 7/treatment). On day 130 of gestation, the remaining ewes were euthanized, and fetal samples were collected. Fetal liver, longissimus dorsi (LD), and blood metabolites were analyzed using LC-MS/MS, and pathway enrichment analysis was conducted using MetaboAnalyst. Then, 600, 518, and 524 metabolites were identified in the liver, LD, and blood, respectively, including 345 metabolites that were present in all three. Nutrient restriction was associated with changes in amino acid, carbohydrate, lipid, and transulfuration/methionine metabolic pathways, some of which were alleviated by realimentation. Fetal age also affected metabolite abundance. The differential abundance of metabolites involved in amino acid, methionine, betaine, and bile acid metabolism could impact fetal epigenetic regulation, protein synthesis, lipid metabolism, and signaling associated with glucose and lipid metabolism. [ABSTRACT FROM AUTHOR]

Poor maternal nutrition (restricted- and overnutrition) during gestation negatively impacts offspring pre- and post-natal growth. Previous work has identified decreased muscle mass and increased adiposity, leading to poor quantity and quality of animal protein products. Alterations in oxidative status, such as the imbalance of antioxidant activity and the production of free radicals, can result in oxidative stress damaging lipid membranes, proteins, and DNA. Changes in oxidative status may contribute to the poor growth outcomes observed in offspring from poorly nourished dams. Therefore, the objective of this research was to determine the effects of poor maternal nutrition during gestation on the oxidative status in offspring skeletal muscle in sheep. We hypothesized that offspring of restricted- and over-fed ewes would have decreased antioxidant activity and increased products of oxidative stress in skeletal muscle. To test this hypothesis, multiparous Dorset ewes (n = 46) pregnant with twins were fed 100% (CON), 60% (RES), or 140% (OVER) of total nutrient requirements (NRC) from d 30 of gestation until parturition. Following parturition, ewes were fed a control diet throughout lactation. At d 282 of age semitendinosus (STN) samples were collected from rams at necropsy, and at d 284 of age muscle biopsies from STN were collected from ewes. Data were analyzed in SAS using PROC MIXED with fixed effects of maternal diet and offspring sex. Data were considered significant at P ≤ 0.05. The activity of the endogenous antioxidant superoxide dismutase (SOD) was decreased by 45% and 33% in RES and OVER offspring, respectively, compared with CON (P ≤ 0.01). Offspring sex did not alter STN SOD activity (P = 0.35). Muscle glutathione peroxidase (GPx) activity was decreased in RES offspring by 20% compared with CON (P ≤ 0.04), but neither differed from OVER offspring (P ≥ 0.24). Ewes had 34% greater GPx activity compared with rams (P < 0.0001). Offspring from RES and OVER ewes had 77% and 87% greater concentrations of malondialdehyde (MDA), a marker of lipid peroxidation, when compared with CON (P < 0.0001). Ewes had 29% greater MDA concentrations compared with rams (P = 0.05). Protein carbonyl (PC), a marker of protein oxidation, concentrations were 36% and 38% greater in RES and OVER offspring, respectively, compared with CON (P ≤ 0.01). The decrease in antioxidant activities and increase in products of protein and lipid oxidation in offspring from poorly nourished dams suggests dysregulation in skeletal muscle oxidative status that may contribute to the negative consequences observed in offspring. Future work should focus on determining the mechanistic role of skeletal muscle oxidative stress in the decreased quantity and quality of animal protein products and identifying potential strategies to mitigate alterations in oxidative status as a result of poor maternal nutrition during gestation. [ABSTRACT FROM AUTHOR]

Restricted nutrition during gestation can reduce offspring productivity. Supplementation of betaine, a methyl donor, promotes fetal growth and liver function. We hypothesized that nutrient restriction during gestation impairs growth, including organ weights and muscle mass, while betaine supplementation would alleviate these negative effects. To determine if maternal betaine supplementation during gestation would improve growth of offspring of restricted-fed dams, multiparous Dorset ewes (n = 47) were estrus synchronized and bred to one of three rams. Ewes confirmed pregnant with twins (n = 32) and singletons (n = 15) were randomly assigned to one of four diets [100% NRC requirements (CON), 60% NRC (RES), CON+betaine (CON+BET; 2 g/d), and RES+BET] from d 30 to 130 of gestation. Among the twins, there were 27 males (CON-8, RES-5, CON+BET-5, and RES+BET-9) and 37 females (CON-8, RES-9, CON+BET-11, and RES+BET-9). Within singletons, there were 7 males (CON-2, RES-2, CON+BET-2, and RES+BET-1) and 8 females (CON-3, RES-1, CON+BET-1, and RES+BET-3). Dam body weight (BW) was measured weekly from d 30 to d 130 of gestation, and diet adjusted accordingly. Dams were euthanized at d 130 of gestation and fetal BW and tissue weights were collected. Data were analyzed using RStudio with P ≤ 0.05 considered significant and 0.05 < P ≤ 0.10 as tendency. At d 130, dams carrying twin fetuses in the CON group were 11.3% and 19.1% heavier than RES and RES+BET dams, respectively (P ≤ 0.05), and CON+BET dams were 18.4% and 10.5% heavier than RES and BET+RES dams, respectively (P ≤ 0.07). However, dams with singletons showed no significant difference in BW (P ≥ 0.37). Regarding fetal BW for singletons, RES fetuses (3.80 ± 0.28kg) were lighter than CON (4.60 ± 0.21kg), CON+BET (4.72 ± 0.27kg), and RES+BET (4.59 ± 0.24kg; P ≤ 0.03). Whereas in twins, RES+BET fetuses (3.19 ± 0.11kg) were lighter than CON (3.68 ± 0.12kg), RES (3.73 ± 0.14kg), and CON+BET (3.60 ± 0.13kg; P ≤ 0.02). In all fetuses, the livers of male RES (28.0 ± 1.49g) and male RES+BET (27.7 ± 1.44g) tended to be heavier than those of female RES+BET (24.5 ± 1.19g; P ≤ 0.07). In terms of muscle mass, female CON+BET (9.33 ± 0.43g) fetuses tended to have greater longissimus muscle (LM) mass compared with female CON (8.30 ± 0.35; P = 0.06), whereas male RES (9.06 ± 0.44g) tended to have heavier LM than male CON+BET (8.02 ± 0.43g; P = 0.09). There were no observed effects of diet, fetal sex, or fetal number on the weights of heart, kidney, perirenal fat, pancreas, semitendinosus muscle, and triceps brachii muscle (P ≥ 0.11). These findings suggest that betaine supplementation may have a significant role in improving fetal BW in singleton pregnancies, with variable effects in twins. Additionally, betaine supplementation may have sex-specific effects on muscle development. [ABSTRACT FROM AUTHOR]

Maternal diet influences offspring growth, but the impact of granddam diet on subsequent generations is less explored. We hypothesized that granddam diet would influence second parity F2 offspring growth. The objective of this study was to determine the influence of granddam diet on second parity F2 offspring growth, morphometric measurements, and organ weights. To determine the impact of poor maternal nutrition of F0 dams on second parity offspring of F1 ewes, multiparous Dorset ewes (F0, n = 46) were fed 100% (control), 60% (restricted), or 140% (over) of NRC requirements from d 30 of gestation until parturition. The F1 ewes (n = 37) were bred at 16 to 19 mo of age to one of two related Dorset rams to generate the first parity F2 generation. The following breeding season, F1 ewes (n = 30) were bred to the same rams to generate the second parity F2 generation offspring (n = 58; F2-2), which were identified as CON F2-2 (n = 6 ewes, 12 rams), RES F2-2 (n = 6 ewes, 12 rams), or OVER F2-2 (n = 9 ewes, 13 rams) corresponding to the diets of the F0 granddams. F2-2 offspring body weights (BW) were recorded weekly from birth (d 0) to d 28, every 14 d until d 126, and every 28 d until d 266 of age. Hip height (HH), crown rump length (CRL), heart girth (HG), and body condition score (BCS) were measured at d 0 and d 120 of age. Rams were necropsied at d 284 ± 0.23. Data were analyzed with R Studio with P ≤ 0.05 considered significant and 0.05 < P ≤ 0.10 considered a tendency. Granddam diet and offspring sex were included in the model with animal ID as a random effect where appropriate. On d 210 and d 238, CON F2-2 tended to weigh 6.8% and 6.3% less, respectively, than OVER F2-2 (P = 0.07) but were not different than RES F2-2 at d 210 (P = 0.55) or d 238 (P = 0.15). We did not detect an effect of granddam diet on HH (P = 0.28), CRL (P = 0.31), or HG (P = 0.62) at birth. At d 120, ewes had 3.1% shorter CRL (P = 0.07) and weighed 9.4% less (P = 0.003) than rams. Immediately before necropsy, CON F2-2 rams tended to have 5.9% less BCS compared with RES F2-2 rams (P = 0.07) and 5.6% less BCS than OVER F2-2 rams (P = 0.10). At necropsy, granddam diet did not influence organ weight. Overfed and restricted granddam diet may increase BW and BCS of second parity, second generation offspring, which provides evidence that maternal diet has multigenerational effects on offspring. [ABSTRACT FROM AUTHOR]

Maternal nutrition during gestation and resulting impacts on ram reproduction and epigenetics are poorly understood. We previously reported altered mRNA and epigenetic markers in F1 ram sperm due to poor maternal diet (restricted- and over-feeding) during gestation, yet the multigenerational effects on ram reproduction are unexplored. We hypothesized that F2 offspring born from restricted- and over-fed granddams would exhibit altered reproductive characteristics, and F1 and F2 offspring would display altered circulating concentrations of reproductive hormones. The objectives of this study were to determine the effects of poor maternal diet on 1) the reproductive function of F2 ram offspring, and 2) key reproductive hormones in F1 and F2 offspring. To evaluate these objectives, multiparous Dorset ewes (F0, n = 46) were fed 100% (CON), 60% (RES), or 140% (OVER) of National Research Council requirements from d 30 of gestation through parturition and a control diet during lactation. Offspring are identified as CON-F1 (n = 10 ewes; 12 rams), RES-F1 (n = 13 ewes; 21 rams), and OVER-F1 (n = 16 ewes; 15 rams). The F1 ewes (n = 37) were maintained on a control diet throughout and were bred between 16 and 19 mo of age to establish the F2 generation. Resulting male offspring are referred to as CON-F2 (n = 6 rams), RES-F2 (n = 13 rams), and OVER-F2 (n = 9 rams) in correspondence to the diets of the granddam. Semen samples of F2 rams were collected via electroejaculation at d 248.4 ± 0.36 (collection 1) and d 255.4 ± 0.36 (collection 2). Semen quality (volume, pH, sperm motility, and sperm concentration) was evaluated at both collections using mCASA; iSperm, Aidmics Biotechnology Co., LTD. Scrotal circumference was measured at collection 2. Sperm morphology was determined by contrast microscopy. Testosterone (T) and follicle stimulating hormone (FSH) were measured in F1 and F2 serum samples collected at d 256 ± 0.13 using commercially available kits. Data were analyzed using R Studio with P ≤ 0.05 considered significant and 0.05 < P ≤ 0.10 considered a tendency. An effect of granddam diet was not observed for F2 ram semen volume, pH, sperm motility, sperm concentration, scrotal circumference, nor histological sperm morphology (P ≥ 0.25). An effect of F0 diet was not observed for F1 or F2 offspring serum concentrations of T and FSH (P ≥ 0.28). In our model, F0 diet during gestation did not affect F2 male offspring sperm quality or circulating T and FSH in F1 and F2 generations. However, based on our previous reports that F0 diet altered F1 sperm epigenome, there may be an impact of maternal diet on epigenetic inheritance which warrants further exploration. [ABSTRACT FROM AUTHOR]

Foals are born with little to no immunity and rely on maternal colostrum to develop adequate circulating immunoglobulin G (IgG) concentrations in the periparturient period. Colostrum directly impacts the health of the foal, and there are limited data assessing how maternal metabolism and body condition impacts IgG in colostrum and in the foal postnatally. To determine the influence of maternal body condition score (BCS) and cresty neck score (CNS) on glucose and insulin metabolism in the pregnant mare, colostrum composition, and colostrum and foal IgG concentrations, light breed mares (n = 6) were divided into two groups based on BCS and CNS at 315 ± 0.45 d of gestation. The groups were identified as moderately obese (MO; n = 3, BCS) and lean (LN; n = 3). Mares were fasted overnight and then underwent an intravenous (iv) glucose tolerance test at 315 ± 0.45 d gestation. Blood samples were collected at -30, -15 and 0 min and mares were administered dextrose iv [0.3 g/kg body weight (BW)] over 3.7 ± 0.17 min followed by an intravenous infusion of insulin (0.3 mU/kg BW) 20-min later. Additional blood samples were collected 2, 5, 10, 15, 20, 25, 30, 45, 60, and 120 min after initiation of dextrose infusion. At parturition, a colostrum sample was collected before foals nursed and analyzed for protein and fat, and IgG concentration. A foal blood sample was collected 18 h after birth to determine passive transfer of IgG. Placental, mare, and foal weights were measured at birth. Data were analyzed using a t-test with significance at P ≤ 0.05 and a tendency at 0.05 < P ≤ 0.10. The MO group had greater BCS (P = 0.01) and CNS (P = 0.01) than the LN group. Moderately obese mares tended to have 9% greater glucose area under the curve (AUC) after dextrose (P = 0.10) and a 9% greater glucose AUC after insulin infusion (P = 0.10) than LN mares. Colostrum IgG concentrations, and protein and fat content (P ≥ 0.3) did not differ between groups. Foal serum IgG concentrations, foal BW, and placental weights were similar between groups (P ≥ 0.8). The ratios between foal BW and placenta weight, and between foal BW and mare BW were similar between groups (P ≥ 0.3). Moderately obese maternal BCS and CNS scores may decrease maternal glucose clearance during late gestation but did not impact colostrum quality or foal IgG concentrations within 24 h postpartum. As the equine fetus matures later in gestation than other livestock species and relies heavily on glucose uptake from the placenta, it is critical to increase our understanding of the impacts of maternal obesity and glucose clearance on foal development and pre- and post-natal health. [ABSTRACT FROM AUTHOR]

Poor maternal nutrition (under- or overfeeding) during gestation negatively impacts antioxidant activity and oxidative stress markers in first generation (F1) offspring. To determine if these alterations persist into subsequent generations, multiparous Dorset ewes (F0; n = 46) pregnant with twins were fed 100% (CON), 60% (RES), or 140% (OVER) of total nutrient requirements (NRC) from d 30 of gestation until parturition. At 16 to 19 mo of age, F1 ewes (n = 37) were maintained on a control diet and bred to generate second generation offspring (F2; CON-F2, RESF2, OVER-F2 corresponding to F0 diet). At 112 and 224 d of age, plasma samples were collected from F2 offspring, and at d 284 semitendinosus (STN) samples were collected from rams at necropsy and muscle biopsies in ewes. Data were analyzed in SAS using PROC MIXED where significance was determined at P ≤ 0.05. Circulating superoxide dismutase (SOD) activity was decreased by 21% and 25% in RES-F2 and OVER-F2 offspring, respectively, compared with CON-F2 (P < 0.0001). Plasma SOD activity was 17% less at d 224 than d 112 (P < 0.0001). Ewes had 9% greater circulating SOD activity compared with rams (P = 0.03). Muscle SOD activity was 31% and 35% greater in CON-F2 compared with RES-F2 and OVER-F2 offspring, respectively (P ≤ 0.003). Rams had 26% greater STN SOD activity than ewes (P = 0.006). Plasma glutathione peroxidase (GPx) activity was 14% greater in CON-F2 than RES-F2 and OVER-F2 offspring (P ≤ 0.003). Circulating GPx activity was 14% less at d 224 than d 112 (P < 0.0001). Muscle GPx activity was 39% and 35% greater in CON-F2 offspring compared with RES-F2 and OVER-F2, respectively (P < 0.0001). Ewes had 11% and 16% greater GPx activity in circulation and STN, respectively, than rams (P ≤ 0.005). Plasma concentrations of malondialdehyde (MDA) were 18% and 10% greater in RES-F2 and OVER-F2 offspring, respectively, than CON-F2 (P = 0.004). Circulating MDA concentrations were 20% greater at d 224 compared with d 112 (P < 0.0001). Concentrations of MDA in STN were increased in RES-F2 and OVER-F2 offspring by 36% and 50%, respectively, compared with CON-F2 (P ≤ 0.006). Ewes had 87% greater concentrations of MDA in STN compared with rams (P < 0.0001). Circulating protein carbonyl (PC) concentrations were 16% greater in RES-F2 offspring than CON-F2 and OVER-F2 (P ≤ 0.04). Plasma PC concentrations were 9% greater at d 224 compared with d 112 (P = 0.04). The concentrations of PC in STN were 81% and 69% greater in RES-F2 and OVER-F2 rams, respectively, compared with CON-F2 rams (P ≤ 0.0001). Alterations in oxidative status persist into the F2 generation and may impact muscle growth and metabolism. [ABSTRACT FROM AUTHOR]

To determine the effects of poor maternal nutrition on the growth and metabolism of offspring into maturity, multiparous Dorset ewes pregnant with twins (n = 46) were fed to either 100% (control; n = 13), 60% (restricted; n = 17), or 140% (over; n = 16) of National Research Council requirements from day 30 ± 0.02 of gestation until parturition. Offspring of these ewes are referred to as CON (n = 10 ewes; 12 rams), RES (n = 13 ewes; 21 rams), or OVER (n = 16 ewes; 13 rams), respectively. Lamb body weights (BW) and blood samples were collected weekly from birth (day 0) to day 28 and then every 14 d until day 252. Intravenous glucose tolerance test (infusion of 0.25 g dextrose/kg BW) was performed at day 133 ± 0.25. At day 167 ± 1.42, individual daily intake was recorded over a 77 d feeding period to determine residual feed intake (RFI). Rams were euthanized at day 282 ± 1.82 and body morphometrics, loin eye area (LEA), back fat thickness, and organ weights were collected. The right leg was collected from rams at necropsy and dual-energy x-ray absorptiometry was used to determine bone mineral density (BMD) and length. Averaged from day 0 until day 252, RES and OVER offspring weighed 10.8% and 6.8% less than CON offspring, respectively (P ≤ 0.02). When adjusted for BW, liver and testes weights tended to be increased and decreased, respectively, in RES rams compared with CON rams (P ≤ 0.08). Additionally, RES BMD and bone length were less than CON rams (P ≤ 0.06). Treatment did not influence muscle mass, LEA, or adipose deposition (P ≥ 0.41). Rams (−0.17) were more feed efficient than ewes (0.23; P < 0.01); however, no effect of maternal diet was observed (P ≥ 0.57). At 2 min post glucose infusion, glucose concentrations in OVER offspring were greater than CON and RES offspring (P = 0.04). Concentrations of insulin in CON rams tended to be greater than OVER and RES ewes at 5 min (P ≤ 0.07). No differences were detected in insulin:glucose or area under the curve (AUC) for glucose or insulin (P ≤ 0.29). Maternal diet did not impact offspring triglycerides or cholesterol (P ≤ 0.35). Pre-weaning leptin tended to be 70% greater in OVER offspring than CON (P ≤ 0.07). These data indicate that poor maternal nutrition impairs offspring growth throughout maturity but does not affect RFI. Changes in metabolic factors and glucose tolerance are minimal, highlighting the need to investigate other mechanisms that may contribute to negative impacts of poor maternal diet. [ABSTRACT FROM AUTHOR]

It is generally well accepted that the pubertal surge in estrogen is responsible for the rapid bone accretion that occurs during puberty and that this effect is mediated by an estrogen-induced increase in growth hormone (GH)/insulin-like growth factor (IGF) action. To test the cause and effect relationship between estrogen and GH/IGF, we evaluated the consequence of ovariectomy (OVX) in prepubertal mice (C57BL/6J mice at 3 wk of age) on skeletal changes and the GH/IGF axis during puberty. Contrary to our expectations, OVX increased body weight (12-18%), bone mineral content (11%), bone length (4%), bone size (3%), and serum, liver, and bone IGF-I (30-50%) and decreased total body fat (18%) at 3 wk postsurgery. To determine whether estrogen is the key ovarian factor responsible for these changes, we performed a second experiment in which OVX mice were treated with placebo or estrogen implants. In addition to observing similar results compared with our first experiment, estrogen treatment partially rescued the increased body weight and bone size and completely rescued body fat and IGF-I levels. The increased bone accretion in OVX mice was due to increased bone formation rate (as determined by bone histomorphometry) and increased serum procollagen peptide. In conclusion, contrary to the known estrogen effect as an initiator of GH/IGF surge and thereby pubertal growth spurt, our findings demonstrate that loss of estrogen and/or other hormones during the prepubertal growth period effect leads to an increase in IGF-I production and bone accretion in mice. osteoporosis; estrogen; puberty; bone size; bone mineral density

Growth hormone (GH) is important in the development and maintenance of bone; however, the IGF-dependent and -independent molecular pathways involved remain to be established. We used microarray analysis to evaluate GH signaling pathways in 4-wk-old GH-deficient mice following a single injection of GH (4 mg/kg body wt) or PBS (n = 6/group) at 6 or 24 h after treatment. Six thousand one hundred sixty genes were differentially expressed at P [less than or equal to] 0.05, and 17% of these genes were identified at both time points. Several of the genes differentially expressed were expressed sequence tags, and the remaining genes fell into 49 Gene Ontology categories. For subsequent studies, we focused on T-box (Tbx)3, a novel transcription factor, which increased more than twofold at both time points. Real-time RT-PCR analysis determined that pretreatment with IGF-binding protein-4 did not block GH-induced Tbx3 expression in vitro. Pretreatment with TNF-[alpha] blocked GH-induced Tbx3 expression. Tbx3 expression increased during osteoblast differentiation and following BMP-7 and Wnt3a treatment (P [less than or equal to] 0.05). Blocking Tbx3 expression by small interfering RNA decreased cell number and [[sup.3.H]]Thymidine incorporation (P < 0.01). In conclusion, 1) GH caused acute changes in several novel genes, suggesting that many GH-induced signaling pathways and target genes remain to be discovered; 2) because Tbx3 expression is regulated in osteoblasts and blockage of Tbx3 expression decreased cell number and DNA synthesis, we propose that Tbx3 is an important determinant of osteoblast cell number. insulin-like growth factor I; lit/lit mouse; signaling pathways

The objective of this study was to determine the effects of poor maternal nutrition (restricted- and over-feeding) during gestation on the reproductive efficiency of female offspring. We hypothesized that ewes born to restricted- and over-fed dams would have reduced fertility and decreased concentrations of follicle stimulating hormone (FSH) and progesterone (P4). Multiparous Dorset ewes (F0; n = 46) were fed one of three diets from d 30 of gestation until parturition according to NRC requirements for total digestible nutrients: control- (100%), restricted- (60%), or over- (140%) fed. Resulting female offspring (F1; n = 38) were raised on a control diet and are identified as CON (n = 10), RES (n = 12), or OVER (n = 16) corresponding to diets of their dam. Between 16 and 19 mo of age, the F1 ewes were estrous synchronized by vaginal insertion of a controlled intravaginal drug release device (CIDR) for a 12-d period, followed by a 2 mL (5 mg/mL) intramuscular injection of prostaglandin F2α, and then bred to one of two related rams. Day 0 of gestation was considered when a raddle mark was observed on the rump of the ewe. Time to pregnancy was calculated as the number of days from when the ewes were initially housed with the ram until d 0 of gestation. Based on ultrasounds on d 37 ± 0.77 of gestation, all F1 ewes were identified as pregnant on first service and number of fetuses was recorded and lambs born were counted at parturition. Data were analyzed using RStudio with a significance of P ≤ 0.05 and a tendency of 0.05 < P ≤ 0.10. Maternal diet did not significantly affect time to pregnancy, number of fetuses, or number of lambs born (P ≥ 0.13). Blood samples (10 mL) were collected via jugular venipuncture at four timepoints (d -14, -7, 0, 7) corresponding to d 0 of gestation and were analyzed for concentrations of FSH and P4 by enzyme-linked immunoassays in 29 ewes (CON: n = 8, RES: n = 8, OVER: n = 13). The CON ewes had 15.2% less FSH than OVER ewes (P = 0.05) and RES ewes tended to have 14.2% less FSH than OVER ewes (P = 0.08). Concentrations of P4 were not different in F1 ewes (P ≥ 0.14). However, concentrations of P4 in F1 ewes tended to increase (P = 0.08) by 12% from d-14 to d 0, which corresponds with a normal estrous cycle. The increased concentration of FSH in OVER ewes could be due to a dysregulation of FSH. However, those effects may be mitigated at some point in time later in gestation since there were no differences in time to pregnancy nor number of lambs born. [ABSTRACT FROM AUTHOR]

Poor maternal nutrition (restricted- and over-feeding) during gestation can negatively impact the efficiency of livestock production by generating offspring with decreased muscle mass, increased adiposity, and impaired metabolism. The mechanisms behind these altered phenotypes are not well-characterized. The effects of poor maternal nutrition during gestation on offspring growth and development begin in utero and contribute to metabolic dysregulation of offspring into maturity and across subsequent generations, demonstrating long-term negative effects on the livestock. Fetal programming results in epigenetic modifications that can involve changes in offspring gene expression and downstream function, with no alteration on the DNA sequence. Using a sheep model of poor maternal nutrition, we have previously shown that F1 offspring from restricted- and over-fed dams are smaller at 10 mo of age relative to offspring from control-fed dams. Additionally, we observed that this phenotype persisted in the F2 offspring from restrictedfed granddams, while F2 offspring from over- and control-fed granddams were of similar body weight. We have recently demonstrated that F1 offspring from poorly nourished ewes have differential methylation patterns and altered gene expression in liver tissue demonstrating a potential mechanism that contributes to persistent altered growth. We have also begun evaluating the effects of maternal nutrient restriction on the development of fetal small intestine, a key facilitator of nutrient transport. Poor maternal nutrition during gestation alters development of offspring small intestine and further understanding of developmental programming in key metabolic tissues can aid in the development of nutritional strategies to improve efficiency of livestock production. [ABSTRACT FROM AUTHOR]