P2-123 Maternal obesity at conception programs obesity in the offspring

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S164 PostersP2-123 Maternal obesity at conception programs obesity in theoffspringK. Shankar1,2 *, A. Harrell1, J.M. Gilchrist1,4, M.J.J. Ronis1,2,T.M. Badger1,2,3. 1Arkansas Childrens Nutrition Center andDepartments of 2Pharmacology and Toxicology, 3Physiology andBiophysics, and 3Pediatrics, University of Arkansas for MedicalSciences, Little Rock, Arkansas, USAThe risk of obesity in adult-life is subject to programming duringgestation.Aims: To examine whether in utero exposure to maternal obesityincreases the risk of obesity in the offspring, we have developedan overfeeding-based model of maternal obesity in rats utilizingintragastric feeding of diets via total enteral nutrition (TEN).Study design: Feeding liquid diets to adult female rats at220 kcal/kg3/4/d (15% excess calories/d) compared to 187 kcal/kg3/4/d(NRC-recommendations) for 3 wks caused substantial increasein body-weight gain, adiposity, serum insulin, leptin and insulinresistance.Subjects: Lean or obese female rats mated with ad libitum AIN-93G-fed male rats. Exposure to obesity was ensured to be limitedonly to the maternal in utero environment by cross-fostering pupsto lean dams having ad libitum access to AIN-93G diets throughoutlactation.Results: Numbers of pups, birth weight and size were notaffected by maternal obesity. Male offspring from each groupwere weaned at PND21 to either AIN-93G diets or high fat diets(HFD, 45% fat calories). Body weights of offspring from obesedams did not differ from offspring of lean dams when fed AIN-93G diets through PND130. However, offspring from obese damsgained remarkably greater (p < 0.005) body weight and higher% body fat when fed HFD. Body composition was assessed by NMR,X-ray computerized tomography and weights of adipose tissues.Adipose histomorphometry and food intake was also assessed inthe offspring.Conclusions: Our data suggest that maternal obesity at conceptionleads to fetal programming of the offspring that could result inobesity in later-life.P2-124 Early embryonic genes regulating adipogenesis arealtered in offspring of cafeteria fed damsS. Sen, T. Ord, C. Williams, R.A. Simmons*. University ofPennsylvania School of Medicine, Childrens Hospital ofPhiladelphia, Philadelphia, PA, USAMaternal obesity signicantly increases fetal and neonatal adiposityand offspring of obese mothers have a very high risk of developingobesity in later life.Aims:1. characterize the phenotype of offspring born to dams fed acafeteria diet;2. determine whether obesity in pregnancy alters expression ofgenes critical to adipogenesis (HoxA5, Gpc4, PPARg, BMP4).Study design: Three groups of animals were studied: (1) femalerats fed a cafeteria diet from the time of weaning until thetime of breeding (approximately 10 weeks of age) (PrePreg);(2) female rats fed a cafeteria diet as above were bred and thediets continued throughout pregnancy prepregancy + pregnancy(Pre+Preg); (3) control animals fed regular rat chow. Pups in allthree groups were cross-fostered to normal female rats. Data wereanalyzed by ANOVA. RNA was isolated from blastocysts (day 5embryo), fat of 2wk and 2mo offspring and analyzed by real-timePCR.Results: There was no signicant difference in food intakebetween groups after approximately 2 3 weeks. Birth weightsof the pups from the 3 groups did not differ and averaged5.090.05, 5.080.05, and 5.100.04 (Con, PrePreg, and Pre+Pregrespectively; n = 10 litters from each group). Despite no differencein body weight, offspring of cafeteria fed maternal rats hadincreased % fat mass at 2 weeks, as determined by DEXA: Con:11.10.5%; PrePreg: 15.30.5*; Pre+Preg: 15.70.6* (*p < 0.05 vs.Con, n = 5 each group). At 6 months of age, adiposity was furtherincreased in the offspring of cafeteria fed dams and was nearly2-fold higher in both treatment groups (p < 0.05, n = 5 each group).GTTs and ITTs at 6 months demonstrated mild glucose intoleranceand insulin resistance in offspring of cafeteria fed dams (p < 0.05,n = 5 each group). PPARg, BMP4, HoxA5 and Gpc4 expression wassignicantly increased in offspring (both blastocysts and postnataloffspring) of cafeteria fed maternal rats (p < 0.05 vs. Con, n = 3 eachgroup).Conclusions: We conclude that exposure to the in uteroenvironment of maternal obesity leads to both phenotypic andgenotypic changes related to adipogenesis in offspring.P2-125 Pregnancy outcomes in primiparous obese women andassociated nutritional factorsS.J. Wheeler1 *, D. Rajasingam2, P.T. Seed2, J. Thomas1,A.L. Briley2, A.H. Shennan2, L. Poston2. 1Nutritional SciencesDivision, Kings College London, Franklin-Wilkins Building, LondonMaternal & Fetal Research Unit, Division of Reproduction andEndocrinology, Kings College London, St Thomas Hospital, London;2Maternal & Fetal Research Unit, Division of Reproductionand Endocrinology, Kings College London, St Thomas Hospital,London, UKE-mail: lucilla.poston@kcl.ac.ukAims: To explore relationships between maternal obesity andpregnancy outcomes and to examine associations betweenpregnancy outcomes and biomarkers of maternal nutritional statusand oxidative stress.Study design: 768 obese, primiparous pregnant women took partin a randomised controlled trial of antioxidant prophylaxis forpre-eclampsia. Subjects provided non-fasting blood samples at14 22 weeks gestation which were analysed for concentrationsof plasma ascorbic acid, retinol, g-tocopherol and a-tocopherol,malondialdehyde, uric acid and lipid proles. Dietary intake wasassessed in 89 subjects who completed 7-day food diaries.Subjects: Recruited from 25 UK hospitals and a hospital inAmsterdam. Control and intervention groups were consideredtogether as the intervention was without effect and bloodwas taken before randomisation. Median BMI was 34.8 kg/m2(IQR: 32.4 38.2).Outcome measures: Pre-eclampsia and birthweight, adjusted formaternal parity, BMI, ethnicity and infant sex and gestationalage. Small-for-gestational age (SGA) babies were dened as


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