Posters Study design: Longitudinal study using a sub-sample from the Birth to Twenty birth-cohort set in Soweto-Johannesburg, South Africa. Subjects: 368 black (African) children (191 boys; 177 girls). Outcome measures: Height, weight, and BMI data collected at 2 3 years and 9 10 years. Overweight was classiï¬ed according to IOTF cut-offs. Results: BMI between at 3 yrs and 10 yrs tracked signiï¬cantly (0.36 boys; 0.40 girls) about the same as height (0.40; 0.37) and not quite as strongly as weight (0.43; 0.58). 40% of children who were overweight at 3 yrs were also overweight at 10 yrs and were 6 times more likely to be overweight at 10 years compared to those of normal BMI at 3 yrs (OR = 6.3, 95% CI 2.9 to 13.5). Those tracking for overweight had signiï¬cantly greater BMI at 3 yrs (18.9 v 18.1 p < 0.01) than those who did not track. Conclusion: Tracking of BMI from 3 to10 years was better than previously published data for early childhood (0.5 7 yrs r = 0.3) but no better than at later childhood ages (6 13 yrs r > 0.6). Whilst 4 out of 10 overweight 3 year-olds will still be overweight at the end of childhood, all overweight 3 year-olds have a signiï¬cantly increased risk of maintaining their overweight status and should be the target of monitoring and intervention programmes. P2-106 The predictors of early adiposity rebound M. Campbell1 *, M. Wake1 , J. Williams1 , J. Carlin2 . 1 Centre for Community Child Health, 2 Clinical Epidemiology and Biostatistics Unit, Murdoch Childrens Research Institute, Royal Childrenâs Hospital (Melbourne), Parkville VIC 3052, Australia E-mail: email@example.com Adiposity rebound (AR) refers to the typical nadir and subsequent steady increase of the Body Mass Index (BMI) that usually occurs between 4 and 7 years of age. While early AR is known to be associated with later obesity, much less is known about determinants of its timing, precluding evidence-based efforts to prevent obesity by delaying onset of AR. Aims: To investigate predictors of early AR from child, parent, nutritional and growth variables collected in the postnatal and preschool period. Study design: Prospective cohort study. Subjects: Community sample of 304 healthy ï¬rst-born children from Melbourne, Australia, followed from 0 6 years, weighed and measured on 13 occasions. Parents completed seven questionnaires from 0 to 2 years, and at 4 years. Outcome measures: Timing of AR was determined by combining visual inspection criteria with modelled (Reed 5-parameter) BMI trajectories. Early AR was deï¬ned as the upward inï¬ection in BMI occurring by age 5 years. Results: The prevalence of early AR was 30%. Multiple logistic regression (adjusted for maternal education) showed the following signiï¬cant predictors of early AR: female gender (OR 2.4; 95% CI 1.3, 4.5), low SES (SEIFA index of disadvantage quintile OR 0.7; 95% CI 0.6, 1.0), and having a greater number of overweight parents (OR 1.8; 95% CI 1.2, 2.9). Exclusive breastfeeding for 4 months had a protective effect (OR 0.5; 95% CI 0.3, 0.9). Conclusions: Factors evident early in the life course appear to be associated with the timing of AR and hence the risk of later obesity. P2-107 Genistein affects adipose tissue deposition in a dose-dependent and gender-speciï¬c manner M. Penza1 , C. Montani1 , M. Jeremic1 , V. Bicelli1 , V. Mazzone1 , A. Maggi2 , L. Ottobrini2 , D. Di Lorenzo1 *. 1 Laboratory of Biotechnology and Department of Diagnostics, Civic Hospital of Brescia, Italy and 2 Centre of Excellence on Neurodegenerative Diseases, University of Milan, 20133 Milan, Italy. The soy isoï¬avone genistein targets adipose tissue and elicits physiological effects that may vary based on dietary intake. We hypothesized that genisteinâs adipose effects are dose and gender dependent. S159 Four-week-old C57BL/6 male and female mice received daily oral doses of genistein (50 200,000 mg/kg/day) or estradiol (E2) (5 mg/kg/day) for 15 days or a diet containing 800 parts per million (ppm) genistein. Genistein increased epididymal and renal fat pad and adipocyte size at doses up to 50,000 mg/kg/day or at 800 ppm in the diet in males but not in females. The alteration in adipocity correlated with changes in peripheral insulin resistance. These treatments increased genistein serum concentrations from 35Â±6 to 103Â±26 nM 12 hours after treatment and lowered plasma triglycerides and cholesterol levels. The 200,000 mg/kg/day genistein dose decreased adipose tissue weight similarly to E2. This genistein dose down-regulated estrogen receptor (b more than a) and progesterone receptor expression and induced estrogen-dependent adipose differentiation factors; it did not change expression of the minimal consensus estrogen responsive element (ERE) in ERE-tK-LUC mice, which was positively modulated in other tissues (e.g., the lung). E2 downregulated almost all examined adipogenic factors. Gene microarray analysis identiï¬ed factors in fat metabolism and obesity-related phenotypes differentially regulated by low and high doses of genistein, uncovering its adipogenic and antiadipogenic actions. The lower dose induced the phospholipase A2 group 7 (PLA2g7) and the phospholipid transfer protein (PLTp) genes; the 200,000 mg/kg/day dose inhibited them. The antiadipogenic action of genistein and downregulation of adipogenic genes required the expression of ERb. In conclusion, nutritional doses of genistein are adipogenic in a gender-speciï¬c manner, while pharmacological doses inhibited adipose deposition. P2-108 Placental insufï¬ciency reduces the expression of leptin and IGF1 mRNA in the perirenal adipose tissue of fetal sheep: a mechanism for altered fat development and obesity J.A. Dufï¬eld1,3 *, T. Vuocolo2 , R. Tellam2 , B.S. Yuen1 , B.S. Muhlhausler3 , I.C. McMillen3 . 1 Discipline of Physiology, School of Molecular and Biomedical Sciences, The University of Adelaide, South Australia 5005, Australia, 2 CSIRO Livestock Industries, Queensland Biosciences Precinct, 306 Carmody Rd., St Lucia 4067, QLD, Australia, 3 Early Origins of Adult Health Research Group, Sansom Research Institute, School of Pharmacy and Medical Sciences, University of South Australia, SA 5005, Australia E-mail: jaime.dufï¬firstname.lastname@example.org Placental restriction (PR) of fetal growth results in a low birth weight and an increased insulin sensitivity and visceral fat mass. We have investigated whether PR results in altered expression of genes involved in adipogenesis/lipogenesis (PPARg, IGF1, IGF1R, IGF2, IGF2R, G3PDH, GAPDH) and adipokine signalling (leptin, adiponectin) in visceral adipose tissue (VAT) before birth. PR was induced by removal of the majority of endometrial caruncles in non pregnant ewes prior to mating. Fetal blood samples were collected from 116d gestation and perirenal adipose tissue collected from PR (n = 8) and control fetuses (n = 9) at 145d. VAT gene expression was measured by qRT-PCR. PR fetuses had a lower weight (PR: 3.05Â±0.32 kg; Control: 5.14Â±0.20 kg; P < 0.0001), mean gestational PO2 (P < 0.0001), plasma glucose (P < 0.01) and insulin concentrations (P < 0.02), than control fetuses. IGF1 mRNA levels were lower in fetal VAT in the PR group (PR: 0.332Â±0.063; Control: 0.674Â±0.098; P < 0.01), however IGF1R, IGF2 and IGF2R mRNA levels were not different between PR and control fetuses. VAT IGF1 mRNA expression was directly related to fetal plasma glucose (P < 0.01, r2 = 0.71) and insulin concentrations (P < 0.05, r2 = 0.64). Leptin mRNA expression in VAT was lower in PR fetuses (PR: 0.071Â±0.008; Control: 0.115Â±0.013; P < 0.05), although there was no difference in adiponectin, G3PDH or GAPDH expression between the 2 groups. Thus there is evidence that restriction of fetal substrate supply is associated with decreased IGF1 and leptin expression in fetal VAT which may contribute to an altered leptin signalling role in the growth restricted new born and the subsequent emergence of increased visceral adiposity.
Early Human Development – Elsevier
Published: Sep 1, 2007
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