P2-107 Genistein affects adipose tissue deposition in a dose-dependent and gender-specific manner

P2-107 Genistein affects adipose tissue deposition in a dose-dependent and gender-specific manner 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 classified according to IOTF cut-offs. Results: BMI between at 3 yrs and 10 yrs tracked significantly (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 significantly 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 significantly 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 Children’s Hospital (Melbourne), Parkville VIC 3052, Australia E-mail: michele.campbell@mcri.edu.au 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 first-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 defined as the upward inflection 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 significant 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-specific 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 isoflavone genistein targets adipose tissue and elicits physiological effects that may vary based on dietary intake. We hypothesized that genistein’s 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 35±6 to 103±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 identified 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-specific manner, while pharmacological doses inhibited adipose deposition. P2-108 Placental insufficiency 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. Duffield1,3 *, 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.duffield@adelaide.edu.au 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: 3.05±0.32 kg; Control: 5.14±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: 0.332±0.063; Control: 0.674±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: 0.071±0.008; Control: 0.115±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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Early Human Development Elsevier

P2-107 Genistein affects adipose tissue deposition in a dose-dependent and gender-specific manner

Loading next page...
 
/lp/elsevier/p2-107-genistein-affects-adipose-tissue-deposition-in-a-dose-dependent-mfcpeTzPts
Publisher
Elsevier
Copyright
Copyright © 2007 Elsevier Ltd
ISSN
0378-3782
D.O.I.
10.1016/S0378-3782(07)70440-1
Publisher site
See Article on Publisher Site

Abstract

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 classified according to IOTF cut-offs. Results: BMI between at 3 yrs and 10 yrs tracked significantly (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 significantly 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 significantly 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 Children’s Hospital (Melbourne), Parkville VIC 3052, Australia E-mail: michele.campbell@mcri.edu.au 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 first-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 defined as the upward inflection 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 significant 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-specific 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 isoflavone genistein targets adipose tissue and elicits physiological effects that may vary based on dietary intake. We hypothesized that genistein’s 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 35±6 to 103±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 identified 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-specific manner, while pharmacological doses inhibited adipose deposition. P2-108 Placental insufficiency 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. Duffield1,3 *, 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.duffield@adelaide.edu.au 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: 3.05±0.32 kg; Control: 5.14±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: 0.332±0.063; Control: 0.674±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: 0.071±0.008; Control: 0.115±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.

Journal

Early Human DevelopmentElsevier

Published: Sep 1, 2007

There are no references for this article.

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off