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Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring

M. A Hyatt, D. S Gardner, S Sebert, V Wilson, N Davidson, Y Nigmatullina, L. L. Y Chan, H Budge, M. E Symonds, Melanie Healy

Reproduction, Volume: 141, Issue: 1, Pages: 119 - 126

Swansea University Author: Melanie Healy

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DOI (Published version): 10.1530/REP-10-0325

Abstract

Maternal nutrition during the period of early organ development can modulate the offspring's ability to metabolise excess fat as young adults when exposed to an obesogenic environment. This study examined the hypothesis that exposing offspring to nutrient restriction coincident with early hepat...

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Published in: Reproduction
ISSN: 1470-1626 1741-7899
Published: 2010
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URI: https://cronfa.swan.ac.uk/Record/cronfa12190
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spelling 2011-10-01T00:00:00.0000000 v2 12190 2012-07-20 Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring 4654b4128fb21d68f98e2abc8538b45a Melanie Healy Melanie Healy true false 2012-07-20 PHAR Maternal nutrition during the period of early organ development can modulate the offspring's ability to metabolise excess fat as young adults when exposed to an obesogenic environment. This study examined the hypothesis that exposing offspring to nutrient restriction coincident with early hepatogenesis would result in endocrine and metabolic adaptations that subsequently lead to increased ectopic lipid accumulation within the liver. Pregnant sheep were fed either 50 or 100% of total metabolisable energy requirements from 30 to 80 days gestation and 100% thereafter. At weaning, offspring were made obese, and at ~1 year of age livers were sampled. Lipid infiltration and molecular indices of gluconeogenesis, lipid metabolism and mitochondrial function were measured. Although hepatic triglyceride accumulation was not affected by obesity per se, it was nearly doubled in obese offspring born to nutrient-restricted mothers. This adaptation was accompanied by elevated gene expression for peroxisome proliferator-activated receptor γ (PPARG) and its co-activator PGC1α, which may be indicative of changes in the rate of hepatic fatty acid oxidation. In contrast, maternal diet had no influence on the stimulatory effect of obesity on gene expression for a range of proteins involved in glucose metabolism and energy balance including glucokinase, glucocorticoid receptors and uncoupling protein 2. Similarly, although gene expressions for the insulin and IGF1 receptors were suppressed by obesity they were not influenced by the prenatal nutritional environment. In conclusion, excess hepatic lipid accumulation with juvenile obesity is promoted by suboptimal nutrition coincident with early development of the fetal liver. Journal Article Reproduction 141 1 119 126 1470-1626 1741-7899 30 11 2010 2010-11-30 10.1530/REP-10-0325 http://www.ncbi.nlm.nih.gov/pubmed/21045167 COLLEGE NANME Pharmacy COLLEGE CODE PHAR Swansea University 2011-10-01T00:00:00.0000000 2012-07-20T11:35:53.5499928 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine M. A Hyatt 1 D. S Gardner 2 S Sebert 3 V Wilson 4 N Davidson 5 Y Nigmatullina 6 L. L. Y Chan 7 H Budge 8 M. E Symonds 9 Melanie Healy 10
title Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
spellingShingle Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
Melanie Healy
title_short Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
title_full Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
title_fullStr Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
title_full_unstemmed Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
title_sort Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring
author_id_str_mv 4654b4128fb21d68f98e2abc8538b45a
author_id_fullname_str_mv 4654b4128fb21d68f98e2abc8538b45a_***_Melanie Healy
author Melanie Healy
author2 M. A Hyatt
D. S Gardner
S Sebert
V Wilson
N Davidson
Y Nigmatullina
L. L. Y Chan
H Budge
M. E Symonds
Melanie Healy
format Journal article
container_title Reproduction
container_volume 141
container_issue 1
container_start_page 119
publishDate 2010
institution Swansea University
issn 1470-1626
1741-7899
doi_str_mv 10.1530/REP-10-0325
college_str Faculty of Medicine, Health and Life Sciences
hierarchytype
hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
url http://www.ncbi.nlm.nih.gov/pubmed/21045167
document_store_str 0
active_str 0
description Maternal nutrition during the period of early organ development can modulate the offspring's ability to metabolise excess fat as young adults when exposed to an obesogenic environment. This study examined the hypothesis that exposing offspring to nutrient restriction coincident with early hepatogenesis would result in endocrine and metabolic adaptations that subsequently lead to increased ectopic lipid accumulation within the liver. Pregnant sheep were fed either 50 or 100% of total metabolisable energy requirements from 30 to 80 days gestation and 100% thereafter. At weaning, offspring were made obese, and at ~1 year of age livers were sampled. Lipid infiltration and molecular indices of gluconeogenesis, lipid metabolism and mitochondrial function were measured. Although hepatic triglyceride accumulation was not affected by obesity per se, it was nearly doubled in obese offspring born to nutrient-restricted mothers. This adaptation was accompanied by elevated gene expression for peroxisome proliferator-activated receptor γ (PPARG) and its co-activator PGC1α, which may be indicative of changes in the rate of hepatic fatty acid oxidation. In contrast, maternal diet had no influence on the stimulatory effect of obesity on gene expression for a range of proteins involved in glucose metabolism and energy balance including glucokinase, glucocorticoid receptors and uncoupling protein 2. Similarly, although gene expressions for the insulin and IGF1 receptors were suppressed by obesity they were not influenced by the prenatal nutritional environment. In conclusion, excess hepatic lipid accumulation with juvenile obesity is promoted by suboptimal nutrition coincident with early development of the fetal liver.
published_date 2010-11-30T03:14:05Z
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score 10.99342