P2-124 Early embryonic genes regulating adipogenesis are altered in offspring of cafeteria fed dams

S164 P2-123 Maternal obesity at conception programs obesity in the offspring K. Shankar1,2 *, A. Harrell1 , J.M. Gilchrist1,4 , M.J.J. Ronis1,2 , T.M. Badger1,2,3 . 1 Arkansas Children’s Nutrition Center and Departments of 2 Pharmacology and Toxicology, 3 Physiology and Biophysics, and 3 Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA The risk of obesity in adult-life is subject to programming during gestation. Aims: To examine whether in utero exposure to maternal obesity increases the risk of obesity in the offspring, we have developed an overfeeding-based model of maternal obesity in rats utilizing intragastric feeding of diets via total enteral nutrition (TEN). Study design: Feeding liquid diets to adult female rats at 220 kcal/kg3/4 /d (15% excess calories/d) compared to 187 kcal/kg3/4 /d (NRC-recommendations) for 3 wks caused substantial increase in body-weight gain, adiposity, serum insulin, leptin and insulin resistance. Subjects: Lean or obese female rats mated with ad libitum AIN93G-fed male rats. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups to lean dams having ad libitum access to AIN-93G diets throughout lactation. Results: Numbers of pups, birth weight and size were not affected by maternal obesity. Male offspring from each group were weaned at PND21 to either AIN-93G diets or high fat diets (HFD, 45% fat calories). Body weights of offspring from obese dams did not differ from offspring of lean dams when fed AIN93G diets through PND130. However, offspring from obese dams gained 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 in the offspring. Conclusions: Our data suggest that maternal obesity at conception leads to fetal programming of the offspring that could result in obesity in later-life. P2-124 Early embryonic genes regulating adipogenesis are altered in offspring of cafeteria fed dams S. Sen, T. Ord, C. Williams, R.A. Simmons *. University of Pennsylvania School of Medicine, Children’s Hospital of Philadelphia, Philadelphia, PA, USA Maternal obesity significantly increases fetal and neonatal adiposity and offspring of obese mothers have a very high risk of developing obesity in later life. Aims: 1. characterize the phenotype of offspring born to dams fed a cafeteria diet; 2. determine whether obesity in pregnancy alters expression of genes critical to adipogenesis (HoxA5, Gpc4, PPARg, BMP4). Study design: Three groups of animals were studied: (1) female rats fed a cafeteria diet from the time of weaning until the time of breeding (approximately 10 weeks of age) (PrePreg); (2) female rats fed a cafeteria diet as above were bred and the diets continued throughout pregnancy prepregancy + pregnancy (Pre+Preg); (3) control animals fed regular rat chow. Pups in all three groups were cross-fostered to normal female rats. Data were analyzed by ANOVA. RNA was isolated from blastocysts (day 5 embryo), fat of 2 wk and 2 mo offspring and analyzed by real-time PCR. Results: There was no significant difference in food intake between groups after approximately 2 3 weeks. Birth weights of the pups from the 3 groups did not differ and averaged 5.09±0.05, 5.08±0.05, and 5.10±0.04 (Con, PrePreg, and Pre+Preg respectively; n = 10 litters from each group). Despite no difference in body weight, offspring of cafeteria fed maternal rats had increased % fat mass at 2 weeks, as determined by DEXA: Con: 11.1±0.5%; PrePreg: 15.3±0.5*; Pre+Preg: 15.7±0.6* (*p < 0.05 vs.

Posters Con, n = 5 each group). At 6 months of age, adiposity was further increased in the offspring of cafeteria fed dams and was nearly 2-fold higher in both treatment groups (p < 0.05, n = 5 each group). GTT’s and ITT’s at 6 months demonstrated mild glucose intolerance and insulin resistance in offspring of cafeteria fed dams (p < 0.05, n = 5 each group). PPARg, BMP4, HoxA5 and Gpc4 expression was significantly increased in offspring (both blastocysts and postnatal offspring) of cafeteria fed maternal rats (p < 0.05 vs. Con, n = 3 each group). Conclusions: We conclude that exposure to the in utero environment of maternal obesity leads to both phenotypic and genotypic changes related to adipogenesis in offspring. P2-125 Pregnancy outcomes in primiparous obese women and associated nutritional factors S.J. Wheeler1 *, D. Rajasingam2 , P.T. Seed2 , J. Thomas1 , A.L. Briley2 , A.H. Shennan2 , L. Poston2 . 1 Nutritional Sciences Division, King’s College London, Franklin-Wilkins Building, London Maternal & Fetal Research Unit, Division of Reproduction and Endocrinology, King’s College London, St Thomas’ Hospital, London; 2 Maternal & Fetal Research Unit, Division of Reproduction and Endocrinology, King’s College London, St Thomas’ Hospital, London, UK E-mail: [email protected] Aims: To explore relationships between maternal obesity and pregnancy outcomes and to examine associations between pregnancy outcomes and biomarkers of maternal nutritional status and oxidative stress. Study design: 768 obese, primiparous pregnant women took part in a randomised controlled trial of antioxidant prophylaxis for pre-eclampsia. Subjects provided non-fasting blood samples at 14 22 weeks’ gestation which were analysed for concentrations of plasma ascorbic acid, retinol, g-tocopherol and a-tocopherol, malondialdehyde, uric acid and lipid profiles. Dietary intake was assessed in 89 subjects who completed 7-day food diaries. Subjects: Recruited from 25 UK hospitals and a hospital in Amsterdam. Control and intervention groups were considered together as the intervention was without effect and blood was taken before randomisation. Median BMI was 34.8 kg/m2 (IQR: 32.4 38.2). Outcome measures: Pre-eclampsia and birthweight, adjusted for maternal parity, BMI, ethnicity and infant sex and gestational age. Small-for-gestational age (SGA) babies were defined as <5th percentile of the reference birthweight distribution. Results: 11.7% of babies were born pre-term and 12.3% were born small-for-gestational age. Both pre-eclampsia (10.7%) and caesarean section rates (42.5%) increased with maternal BMI (p < 0.001), as did plasma uric acid concentrations (p < 0.001) and g-tocopherol:a-tocopherol ratio (p < 0.001). Pre-eclampsia was associated with plasma triglycerides (p < 0.0001) and low plasma ascorbic acid (p = 0.005). Energy-adjusted sucrose intake was associated with SGA birth (p = 0.034) and lower birthweight centile (p = 0.039). Conclusions: Pregnancy outcomes worsen with increasing obesity. High proportions of sucrose-containing foods in the maternal diet were negatively associated with birthweight, possibly due to the lower glycaemic index of sucrose-rich foods relative to starchy staples. The Vitamins in Pre-eclampsia (VIP) Study was funded by the Wellcome Trust; additional studies are funded by Tommy’s the Baby Charity. P2-126 Evaluation of the effect on simple obesity of children among nursery schools in Shanghai City J.-f. Zhang *, Q. Gong, B.-h. Fang, G.-y. Yao, M. Wei, Y. Jin, L.-j. Yuan. Shanghai Children’s Hospital, Jiaotong University, China Objective: To analyse the rate on simple obesity of children among all nursery schools in Shanghai City, it was evaluated about the