Effects Of Poor Maternal Nutrition Research Articles

PSVI-14 Effects of poor maternal nutrition during gestation on first generation offspring oxidative status in skeletal muscle

Abstract Poor maternal nutrition (restricted- and over-nutrition) 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.

437 Fetal Programming in Sheep: Epigenetic modifications in offspring from poorly nourished dams

Abstract 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 restricted-fed 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.

PSVI-10 Effects of Poor Maternal Nutrition During Gestation on Offspring Basal Immune Status

Abstract Poor maternal nutrition during gestation affects offspring pre- and post-natal growth, decreasing muscularity and increasing adiposity. Chronic inflammation may be a potential mechanism for the alterations reported. The objective of this research was to determine the effects of poor maternal nutrition during gestation on offspring inflammatory status. We hypothesized that offspring of restricted- and over-fed ewes would have an altered inflammatory status which would be dependent on offspring sex. To test this hypothesis, multiparous Dorset ewes (n = 45) pregnant with twins were fed 100% (CON), 60% (RES), or 140% (OVER) of National Research Council requirements from d 30 of gestation until parturition. At parturition, all ewes were fed a control diet, such that the nutritional insult only occurred during gestation. At d 120, whole blood was collected from offspring and RNA was isolated to evaluate 86 genes related to the innate and adaptive immune responses. Data were analyzed in SAS 9.4 using PROC MIXED with fixed effects of offspring sex, maternal diet, and the interaction. Maternal diet affected 7 genes. Bovine major histocompatibility complex, a gene in the innate immune response, was downregulated by 27% and 37% in OVER compared with CON and RES, respectively (P = 0.001). Cluster of differentiation 86, a marker of T cell activation, was upregulated by 17% in OVER compared with CON (P = 0.04). Lymphocyte antigen 96, critical in the response to pathogens, expression was 48% greater in RES compared with CON (P = 0.04). A transcription factor in cytokine signaling, Signal transducer and activator of transcription 3 was upregulated in OVER and RES offspring by 19 and 21%, respectively, compared with CON (P = 0.02). Pattern recognition receptors Toll-like receptor-1 (TLR1), TLR4, and TLR8 were upregulated in RES and OVER compared with CON (P ≤ 0.04). The interaction of offspring sex and maternal diet significantly altered gene expression in 2 genes. A regulator of T cell differentiation, GATA Binding Protein 3 was downregulated in OVER females by 21 to 43% compared with all other offspring and was upregulated in OVER males by 26 to 76% compared with all female offspring (P = 0.04). A gene related to cytokine signaling, Janus Kinase 2 was upregulated in RES and OVER males by 29 to 64% compared with all other offspring (P = 0.05). Sex altered gene expression of 54 genes (P ≤ 0.05). Overall, maternal diet altered gene expression of the innate and adaptive immune responses in a sex-specific manner. Alterations in inflammatory status may contribute to altered body composition and may predispose offspring to impaired response to immune challenges. Future work should focus on the impacts of poor maternal nutrition during gestation on the response to an immune challenge.

PSVIII-25 Investigating the Effects of Poor Maternal Nutrition on F2 Offspring Growth, Residual Feed Intake, and Glucose Tolerance

Abstract Poor maternal nutrition impairs F1 offspring growth independent of changes in feed efficiency and glucose tolerance. To determine if poor maternal nutrition in F0 ewes contributes to F2 offspring growth, feed efficiency, and glucose tolerance, multiparous Dorset ewes (F0; n = 46) pregnant with twins were fed 100% (control), 60% (restricted) or 140% (over) of NRC requirements from d 30 of gestation until parturition. At 16 to 19 mo of age, female F1 (n = 37) offspring were bred to one of two related Dorset rams to generate F2 offspring, identified as CON-F2 (n = 12 ewes; 6 rams), RES-F2 (n = 7 ewes; 13 rams), or OVER-F2 (n = 13 ewes; 9 rams), corresponding to diets of the granddam. F2 offspring body weight (BW) was measured weekly from birth (d 0) to d 28 and every 14 d until d 252. From d 0 to 70, granddam diet did not influence F2 BW (P ≥ 0.18). However, from d 84 to d 154, RES-F2 tended to be 9.42% lighter than CON-F2 with OVER-F2 intermediate (P ≤ 0.08), and from d 224 to d 252 RES-F2 tended to be 6.47% and 6.29% lighter than CON-F2 and OVER-F2, respectively (P ≤ 0.07). Overall, F2 rams were 8.36 kg heavier than F2 ewes (P < 0.0001). At d 133 ± 0.28 an intravenous glucose tolerance test (0.25 g/kg BW of a 50% dextrose solution) was performed. Glucose and insulin concentrations were determined using commercial kits. Granddam diet did not influence glucose or insulin average or baseline concentrations, area under the curve, first-phase response, or ratio (P ≥ 0.52). However, granddam diet influenced glucose peak response in rams, where CON-F2 rams (297 ± 16.5 mg/dL) had greater glucose peak compared with RES-F2 rams (239 ± 11.2 mg/dL; P = 0.05). At d 167 ± 0.33, daily intake of a complete pelleted feed was recorded using Super SmartFeeders over a 77-day feeding period. A treatment by sex interaction was detected for F2 offspring residual feed intake (RFI; P = 0.08) where CON-F2 ewes (0.31 ± 0.12 kg/d) tended to be less feed efficient than CON-F2 rams (-0.45 ± 0.20 kg/d) and RES-F2 rams (-0.20 ± 0.13 kg/d). Alternately, OVER-F2 ewes (0.16 ± 0.13 kg/d), OVER-F2 rams (0.02 ± 0.15 kg/d), RES-F2 ewes (-0.06 ± 0.18 kg/d), and RES-F2 rams were all of similar (P ≥ 0.34) feed efficiency. Rams were euthanized at d 285 ± 0.93 and body morphometrics, and organ weights were collected. No effect of granddam diet (P ≥ 0.25) on F2 ram morphometric measurements, organ weights, or muscle weights (P ≥ 0.15) were detected at time of necropsy. These data indicate that nutrient restriction during gestation decreases F2 offspring BW independent of RFI and glucose tolerance.

446 The Effects of Maternal Diet During Gestation on Oxidative Status of Offspring

Abstract Poor maternal nutrition during gestation is common in livestock production and includes both nutrient restriction and over-nutrition. Poor maternal nutrition affects offspring pre- and post-natal growth including decreases in muscularity and increases in adiposity which results in poor quantity and quality of animal products. Oxidative stress, when free radicals exceed the capacity of antioxidants, damages lipid membranes, proteins, and DNA. Oxidative stress 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 offspring circulating oxidative status in sheep. We hypothesized that offspring of restricted- and over-fed ewes would have an altered oxidative status in circulation. To test this hypothesis, multiparous Dorset ewes (n = 45) pregnant with twins were fed 100% (CON), 60% (RES), or 140% (OVER) of National Research Council requirements from d 30 of gestation until parturition. At parturition, ewes were fed a control diet such that the nutritional insult only occurred during gestation. Blood samples were collected from offspring by jugular venipuncture at d 112 and d 224 of age to evaluate oxidative status in circulation. Data were analyzed in SAS 9.4 using PROC MIXED with fixed effects of offspring sex and maternal diet with sampling timepoint as repeated measure. Data were considered significant at P < 0.05. In offspring plasma, superoxide dismutase, an endogenous antioxidant, activity was 17% greater in CON offspring compared with RES and OVER (P ≤ 0.04). Malondialdehyde (MDA), a marker of lipid peroxidation, concentration was not different at d 112 but RES animals had 10% lesser concentration of MDA than CON at d 224 (P ≤ 0.02). Protein carbonyl (PC), a marker of protein oxidation, concentration was 9% greater in CON animals than RES and OVER (P = 0.01). Additionally, PC concentrations were 19% greater at d 224 compared with d 112 (P ≤ 0.001). These results indicate that at the chosen timepoints, RES and OVER offspring had less antioxidant activity but also less indication of oxidative damage. Overall, the alterations in antioxidant activity and oxidative damage suggest dysregulation in circulating oxidative status that may contribute to the negative consequences of poor maternal nutrition during gestation. Future work should focus on the impacts of poor maternal nutrition on oxidative stress in muscle.

PSIV-1 Effects of Poor Maternal Nutrition During Gestation on F0 and F1 Ewe Colostrum and Milk Composition and Colostrum Igg

Abstract High-quality colostrum and milk are critical for proper neonatal growth and immune system development. Immunoglobulin G (IgG) is the predominant antibody class in colostrum and is vital for passive immune transfer in sheep. There is limited understanding of how poor maternal nutrition during gestation (restricted- and over-feeding) might influence colostrum and milk composition and colostrum IgG concentrations and how F1 offspring colostrum and milk are impacted as a result of F0 maternal diet. The objective of this experiment was to determine if poor maternal nutrition during gestation impacts F0 and F1 colostrum and milk composition, including IgG concentrations. We hypothesized that maternal restricted-feeding would decrease, and maternal over-feeding would increase total solids, fat, and protein during early and transitional lactation and that restricted-feeding would increase IgG concentrations and over-feeding would decrease IgG concentrations in F0 and F1 ewe colostrum. Multiparous Dorset ewes pregnant (n = 46) with twins were fed 100% (control; n = 13), 60% (restricted; n = 17) or 140% (over; n = 16) of National Research Council (NRC) requirements. After birth and during lactation, dams were fed 100% NRC for lactating ewes, so the nutritional insult only occurred during gestation. Resulting ewe offspring (n = 32) were raised on control diets and were bred between 16 and 19 mo of age. Colostrum samples were collected within 24 h of parturition and milk samples were collected at d 3 and d 21 postpartum. Colostrum and milk composition were evaluated using Brix Refractometry (total solids, g/dL) and spectrophotometry (crude fat, %; crude protein, %). Additionally, a radial immunodiffusion assay was used to determine IgG concentrations (mg/dL) in colostrum. A treatment by time interaction was observed for F0 colostrum crude fat where restricted-fed ewes had less fat than control-fed ewes (P ≤ 0.024). No interaction was detected for all other F0 and F1 composition variables (P ≥ 0.16). We did not detect a main effect of diet on F0 or F1 total solids, crude fat, and crude protein of colostrum nor milk (P ≥ 0.24). A main effect of time was observed for all variables where colostrum had greater total solids, crude fat, and crude protein compared with milk at d 3 and d 21 (P ≤ 0.0001). No effect of maternal diet on IgG concentrations were detected in F0 or F1 ewe colostrum (P ≥ 0.46). These data indicate that poor maternal diet has minimal effects on F0 and F1 ewe colostrum composition and IgG concentrations, and d 3 and d 21 milk composition. In addition, the impact of F0 diet on colostrum fat composition did not persist into the F1 generation.

Restricted- and over-feeding during gestation decreases growth of offspring throughout maturity.

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.

119 Randel Lectureship: The Role of Maternal Nutrition in Developmental Programming Using a Sheep Model

Abstract Appropriate nutrition during gestation is critical for optimal fetal development and life-long health. Poor nutrition during gestation, defined as excess or restricted nutrition, can lead to altered growth and metabolic dysregulation in the offspring. Using a sheep model, we have demonstrated that both restricted- and over-feeding alter offspring growth, impair muscle growth, increase fat accumulation, alter circulating growth and metabolic hormones, and alter mRNA expression of genes involved in myogenesis, lipogenesis, inflammation, and glycogen metabolism. More importantly, these negative impacts of poor maternal nutrition persist through adulthood, and can be passed to subsequent generations. Using omics approaches, we have begun to elucidate the mechanisms by which maternal diet impacts developmental programming and contributes to these persistent effects. In offspring from restricted-fed mothers, fetal liver and muscle morphology demonstrated impaired growth and alterations in key metabolites in methionine, betaine, and bile salt pathways. In offspring from both restricted- and over-fed mothers, global metabolomics demonstrated altered lipid and protein metabolism profiles. These changes in metabolites likely contribute to maternal programming of offspring growth and metabolism including efficiency of energy utilization. In addition to changes in key genes involved in growth, lipid accretion, and protein synthesis, preliminary studies suggest these persistent effects may be due to changes epigenetic regulation in offspring. Using the sheep model of both restricted- and over-feeding we, and others, have demonstrated that the negative effects of poor maternal nutrition affect multiple key metabolic tissues during fetal development and that these changes persist into maturity. Therefore, the focus of our current studies is to determine the multigenerational impacts of poor maternal nutrition on offspring growth and health and elucidate the mechanisms that contribute to these persistent changes.

PSIII-24 Poor gestational nutrition impacts sheep offspring growth but not feed efficiency

Abstract The objective was to determine the effects of poor maternal nutrition during gestation on growth and feed efficiency of offspring. We hypothesized that body weights (BW) would decrease and residual feed intake (RFI) would increase (reduced feed efficiency) in offspring of restricted- and over-fed ewes. Forty-six multiparous Dorset ewes pregnant with twins were fed 100%, 60% or 140% of NRC requirements from d 30 of gestation until parturition. Offspring are referred to as CON (n = 10 ewes; 12 rams), RES (n = 13 ewes; 21 rams), and OVER (n = 16 ewes; 13 rams), respectively. Lamb BW were measured weekly from birth to d 28 and biweekly until d 252 of age. Starting at d 167±13.6, daily intake of a complete pelleted feed was recorded using a Super SmartFeed (C-lock Inc., Rapid City, SD) over a 77 d- feeding period. Average BW were taken two days before, at mid-point, and two days after the feeding trial period and RFI was calculated for each animal. Rams were euthanized at d 284±12 and body morphometrics, loin eye area (LEA), back fat thickness, and organ weights were collected. From birth to d 252, ram lambs were 5.4 kg heavier (P &amp;lt; 0.001) than ewe lambs. Control ewe lambs were 4.3 kg heavier than RES and OVER (P &amp;lt; 0.05) from birth to 9 months and CON rams were 4.7 kg heavier (P &amp;lt; 0.01) than RES. Rams (-0.17) were more efficient than ewes (0.23; P &amp;lt; 0.01); however, no dietary treatment difference was observed (P ≥ 0.57). No differences in muscle mass, LEA, and adipose deposition were observed (P ≥ 0.41). These data indicate that poor maternal diet during gestation impacts offspring growth but not RFI. Further investigation is warranted to determine if differences in BW are a result of metabolic alterations impacted by poor maternal nutrition during gestation.

106 The Effects of Fetal Programming on Offspring Pancreas DNA Methylation

Abstract It has been well documented that fetal programming, caused by changes to the maternal environment during pregnancy, can impact the overall health and growth of the offspring in livestock and non-livestock species alike. These effects are observed in the F1 offspring as well as across subsequent generations; however, the mechanisms by which this occurs are still poorly understood. Epigenetics is one of the many mechanisms that is hypothesized to have a role in fetal programming and may be mediating the observed effects across multiple generations. It has been demonstrated by others that DNA methylation patterns can be altered by an individuals’ diet and that the pancreas is vulnerable to the effects of fetal programming. Therefore, we evaluated the effects of poor maternal nutrition during gestation on the pancreas tissue of lambs. We have demonstrated that maternal under- or overnutrition during gestation alters the DNA methylation patterns of the offspring pancreas tissue with these effects being diet dependent and sex specific. We have also begun evaluating the effects of maternal diet in murine models using whole-genome bisulfite sequencing to compare species differences and determine if there are any changes conserved across species. This will allow us to focus on a smaller number of critical factors in individuals as they age and across multiple generations in livestock species such as sheep and cattle. From these data we will be able to elucidate the role DNA methylation has in mediating the effects of maternal programming in the pancreas tissue.

Effects of poor maternal nutrition during gestation on ewe and offspring plasma concentrations of leptin and ghrelin

Poor maternal nutrition during gestation can negatively affect offspring growth, development, and health. Leptin and ghrelin, key hormones in energy homeostasis and appetite control, may mediate these changes. We hypothesized that restricted- and over-feeding during gestation would alter plasma concentrations of leptin and ghrelin in ewes and offspring. Pregnant ewes (n = 37) were fed 1 of 3 diets starting on d 30 ± 0.02 of gestation until necropsy at d 135 of gestation or parturition: restricted- [RES; 60% National Research Council (NRC) requirements for total digestible nutrients, n = 13], control- (CON; 100% NRC, n = 11), or over-fed (OVER; 140% NRC, n = 13). Blood samples were collected from pregnant ewes at days 20, 30, 44, 72, 100, 128, and 142 of gestation. Offspring blood samples were collected within 24 h after birth (n = 21 CON, 25 RES, 23 OVER). Plasma leptin and ghrelin concentrations were determined by RIA. Ewe data were analyzed using the MIXED procedure in SAS with ewe as the repeated subject. Offspring data were analyzed using the MIXED procedure. Correlations between BW and leptin and ghrelin concentrations were identified using PROC CORR. At d 100, RES (5.39 ± 2.58 ng/mL) had decreased leptin concentrations compared with OVER (14.97 ± 2.48 ng/mL; P = 0.008) and at d 128, RES (6.39 ± 2.50 ng/mL) also had decreased leptin concentrations compared with OVER (13.61 ± 2.47 ng/mL; P = 0.04). At d 142, RES (0.26 ± 0.04 ng/mL) had increased ghrelin concentrations compared with CON (0.15 ± 0.04 ng/mL; P = 0.04). Leptin and ghrelin concentrations were also altered between days of gestation within a dietary treatment. In CON ewes, plasma concentrations of leptin were increased at d 30 (19.28 ± 7.43 ng/mL) compared with d 44 (5.20 ± 3.10 ng/mL; P = 0.03), and the plasma concentrations of ghrelin at d 128 (0.20 ± 0.03 ng/mL) were increased compared with d 30 (0.16 ± 0.03 ng/mL; P = 0.01) and d 100 (0.17 ± 0.03 ng/mL; P = 0.04). Maternal diet did not alter plasma ghrelin or leptin concentrations in the offspring (P > 0.50). There were no strong, significant correlations between ewe BW and leptin (r < 0.33; P > 0.06) or ghrelin (r > -0.47; P > 0.001) concentrations or lamb BW and leptin or ghrelin concentrations (r > -0.32, P > 0.06). Maternal alterations in circulating leptin and ghrelin may program changes in energy balance that could result in increased adiposity in adult offspring. Alterations in energy homeostasis may be a mechanism behind the long-lasting changes in growth, body composition, development, and metabolism in the offspring of poorly nourished ewes.

PSIV-28 Program Chair Poster Pick: The Effects of Poor Maternal Nutrition During Gestation on Ewe and Offspring Plasma Concentrations of Leptin and Ghrelin

Abstract Poor maternal nutrition (restricted- and over-feeding) during gestation may alter leptin and ghrelin, key hormones in energy homeostasis and appetite control. They may also have a regulatory role in maternal metabolic adaptations critical during gestation to ensure optimal offspring growth and development. We hypothesized that restricted- and over-feeding during gestation would alter plasma concentrations of leptin and ghrelin in ewes and their offspring. Pregnant Western White-faced ewes were individually fed 60% (RES; n = 13), 100% (CON; n = 11), or 140% (OVER; n = 13) of NRC requirements for TDN starting on d 30±0.02 of gestation. Blood samples were collected in the morning from fasted pregnant ewes weekly from d 20 of gestation until parturition and from offspring (n = 31) within 24 hours after birth. Leptin and ghrelin concentrations were determined by radioimmunoassay. Data were analyzed using the MIXED procedure in SAS with main effects of treatment, day of gestation and their interaction. Leptin (P &amp;lt; 0.002) and ghrelin (P &amp;lt; 0.015) concentrations were altered in pregnant ewes between treatments within a day of gestation. At d 100 (P = 0.008) and d 128 (P = 0.04), RES ewes (5.392.58 ng/mL; 6.392.50 ng/mL) had decreased leptin concentrations compared with OVER ewes (14.972.48 ng/mL; 13.612.47 ng/mL), with CON ewes intermediate. RES ewes (0.260.04 ng/mL) had increased ghrelin concentrations compared with CON ewes at d 142 (0.150.04 ng/mL; P = 0.042), with OVER ewes intermediate. Leptin (P &amp;lt; 0.002) and ghrelin (P &amp;lt; 0.015) concentrations were altered between days of gestation within a dietary treatment. Leptin concentration increased across gestation in OVER ewes. In RES ewes, leptin concentration decreased and ghrelin concentration increased over gestation. Leptin (P = 0.5) and ghrelin (P = 0.5) concentrations in lambs were not different at birth. Alterations in leptin and ghrelin in ewes during gestation may disrupt critical metabolic adaptations that may contribute to suboptimal offspring growth and development.

Maternal Restricted- and Over-Feeding During Gestation Result in Distinct Lipid and Amino Acid Metabolite Profiles in the Longissimus Muscle of the Offspring.

Maternal over- and restricted-feeding during gestation have similar negative consequences for the offspring, including decreased muscularity, increased adiposity, and altered metabolism. Our objective was to determine the effects of poor maternal nutrition during gestation (over- and restricted-feeding) on the offspring muscle metabolite profile. Pregnant ewes (n = 47) were fed 60% (RES), 100% (CON), or 140% (OVER) of NRC requirements starting at day 30.2 ± 0.2 of gestation. Offspring sample collection occurred at days 90 and 135 of gestation, and within 24 h of birth. C2C12 myoblasts were cultured in serum collected from offspring at birth (n = 18; 6 offspring per treatment) for analysis of oxidative and glycolytic capacity. Unbiased metabolite analysis of longissimus muscle samples (n = 72; 8 fetuses per treatment per time point) was performed using mass spectrometry. Data were analyzed by ANOVA for main effects of treatment, time point, and their interaction. Cells cultured in serum from RES offspring exhibited increased proton leak 49% (p = 0.01) compared with CON, but no other variables of mitochondrial respiration or glycolytic function were altered. Mass spectrometry identified 612 metabolites. Principle component analysis identified day of gestation as the primary driver of metabolic change; however, maternal diet also altered the lipid and amino acid profiles in offspring. The abundance of 53 amino acid metabolites and 89 lipid metabolites was altered in RES compared with CON (p ≤ 0.05), including phospholipids, sphingolipids, and ceramides within the lipid metabolism pathway and metabolites involved in glutamate, histidine, and glutathione metabolism. Similarly, abundance of 63 amino acid metabolites and 70 lipid metabolites was altered in OVER compared with CON (p ≤ 0.05). These include metabolites involved in glutamate, histidine, lysine, and tryptophan metabolism and phosphatidylethanolamine, lysophospholipids, and fatty acids involved in lipid metabolism. Further, the amino acid and lipid profiles diverged between RES and OVER, with 69 amino acid and 118 lipid metabolites differing (p ≤ 0.05) between groups. Therefore, maternal diet affects metabolite abundance in offspring longissimus muscle, specifically metabolites involved in lipid and amino metabolism. These changes may impact post-natal skeletal muscle metabolism, possibly altering energy efficiency and long-term health.

PSXII-15 Effects of poor maternal nutrition during gestation on oxidative stress in offspring muscle.

PSXII-15 Effects of poor maternal nutrition during gestation on oxidative stress in offspring muscle.

442 Effects of poor maternal nutrition during gestation on the offspring muscle metabolome.

442 Effects of poor maternal nutrition during gestation on the offspring muscle metabolome.

PSXII-25 The Effects of Poor Maternal Nutrition on Fetal Brain Development.

PSXII-25 The Effects of Poor Maternal Nutrition on Fetal Brain Development.

A cross-sectional survey investigating women\u2019s information sources, behaviour, expectations, knowledge and level of satisfaction on advice received about diet and supplements before and during pregnancy

BackgroundThe reported long-term effects of poor maternal nutrition and uptake of recommended supplements before and during pregnancy was the impetus behind this study. Our objectives were to investigate and understand women’s expectations, knowledge, behaviour and information sources used regarding the use of nutrition and vitamin supplements before and during pregnancy.MethodsA cross-sectional survey using a self-administered questionnaire was undertaken. A purposive sampling technique was used. Women attending the antenatal clinic at Croydon University Hospital during 2015 were invited to take part in the study. The data was analysed using descriptive statistics, paired sample T-tests and Chi-squared tests, with the level of significance set at 5% (p < 0.05).ResultsA total of 133 pregnant women completed the survey. Analysis of the results showed that women are currently using electronic resources (33%, n = 42) rather than healthcare professionals (19%, n = 25) as an information source before pregnancy. Women who sourced information through the internet were significantly more likely to take folic acid (p = 0.006) and vitamin D (p = 0.004) before pregnancy. Women preferred to receive information from the antenatal clinic (62%, n = 83), internet (46%, n = 61) and from mobile applications (27%, n = 36). Although women believed they had sufficient knowledge (60%, n = 80) and had received adequate advice (53%, n = 70) concerning the correct supplements to take, this was not demonstrated in their behaviour, with only a small number of women (37%, n = 49) taking a folic acid supplement before pregnancy. Women mistakenly perceived the timing of supplement advice as correct, with only a small number of women (18%, n = 23) considering the advice on supplements as too late.ConclusionsDespite the small sample size, this study demonstrated that women did not receive timely and/or accurate advice to enable them to take the recommended supplements at the optimal time. Women had the misconception that they understood the correct use of pregnancy supplements. This misunderstanding may be prevented by providing women intending to become pregnant with a structured, approved electronic source of information that improves their supplements uptake.

Resveratrol Intake During Pregnancy and Lactation Modulates the Early Metabolic Effects of Maternal Nutrition Differently in Male and Female Offspring.

Poor maternal nutrition can have detrimental long-term consequences on energy homeostasis in the offspring. Resveratrol exerts antioxidant and antiobesity actions, but its impact during development remains largely unknown. We hypothesized that resveratrol intake during pregnancy and lactation could improve the effects of poor maternal nutrition on offspring metabolism. Wistar rats received a low-fat diet (LFD; 10.2% kcal from fat) or high-fat diet (HFD; 61.6% kcal from fat), with half of each group receiving resveratrol in their drinking water (50 mg/L) during pregnancy and lactation. Body weight (BW) of dams was measured at treatment onset and weaning [postnatal day (PND) 21] and of pups at birth and PND21, at which time dams and pups were euthanized. Although HFD dams consumed more energy, their BW at the end of lactation was unaffected. Mean litter size was not modified by maternal diet or resveratrol. At birth, male offspring from HFD and resveratrol (HFD + R) dams weighed less than those from LFD and resveratrol (LFD + R) dams. On PND21, pups of both sexes from HFD dams weighed more, had more visceral adipose tissue (VAT) and subcutaneous adipose tissue (SCAT), and had higher serum leptin levels than those from LFD dams. Resveratrol reduced BW, leptin, VAT, and SCAT, with females being more affected, but increased glycemia. Neuropeptide levels were unaffected by resveratrol. In conclusion, resveratrol intake during pregnancy and lactation decreased BW and adipose tissue content in offspring of dams on an HFD but did not affect offspring from LFD-fed dams, suggesting that the potential protective effects of resveratrol during gestation/lactation are diet dependent.

075 Effects of poor maternal nutrition and gender on satellite cell metabolism in lambs

075 Effects of poor maternal nutrition and gender on satellite cell metabolism in lambs

082 The effects of poor maternal nutrition during gestation on the number of Pax7-positive myogenic progenitor cells

082 The effects of poor maternal nutrition during gestation on the number of Pax7-positive myogenic progenitor cells