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Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity

L. L. Y Chan, S. P Sebert, M. A Hyatt, T Stephenson, H Budge, M. E Symonds, D. S Gardner, Melanie Healy

AJP: Regulatory, Integrative and Comparative Physiology, Volume: 296, Issue: 5, Pages: R1455 - R1463

Swansea University Author: Melanie Healy

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DOI (Published version): 10.1152/ajpregu.91019.2008

Abstract

Maternal nutrient restriction (NR) from early to midgestation has marked effects on endocrine sensitivity and organ function of the resulting offspring. We hypothesized that early NR may reset the expression profile of genes central to myocardial energy metabolism, influencing ectopic lipid depositi...

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Published in: AJP: Regulatory, Integrative and Comparative Physiology
ISSN: 0363-6119 1522-1490
Published: 2009
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URI: https://cronfa.swan.ac.uk/Record/cronfa12196
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spelling 2011-10-01T00:00:00.0000000 v2 12196 2012-07-20 Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity 4654b4128fb21d68f98e2abc8538b45a Melanie Healy Melanie Healy true false 2012-07-20 MEDS Maternal nutrient restriction (NR) from early to midgestation has marked effects on endocrine sensitivity and organ function of the resulting offspring. We hypothesized that early NR may reset the expression profile of genes central to myocardial energy metabolism, influencing ectopic lipid deposition and cardiac function in the obese adult offspring. NR offspring were exposed to an "obesogenic" environment, and their cardiac function and molecular indexes of myocardial energy metabolism were assessed to explore the hypothesis that an obese individual's risk of heart disease may be modified after maternal NR. Pregnant sheep were fed 100% (control) or 50% (NR) energy requirement from days 30 to 80 of gestation and 100% energy requirement thereafter. At weaning, offspring were exposed to an obesogenic environment or remained lean. At approximately 1 yr of age, the hemodynamic response of these offspring to hypotension, together with left ventricular expression profiles of fatty acid-binding protein 3 (FABP3), peroxisome proliferator-activated receptor-gamma (PPARgamma) and its coactivator (PGC)-1alpha, acetyl-CoA carboxylase (ACC), AMP-activated protein kinase (AMPK)-alpha(2), and voltage-dependent anion channel 1 (VDAC1), was determined. Obesity produced left ventricular hypertrophy in all animals, with increased ectopic (myocardial) lipid in NR offspring. Obesity per se significantly reduced myocardial transcript expression of PGC-1alpha, AMPKalpha(2), VDAC1, and ACC and increased expression of PPARgamma and FABP3. However, although NR animals were similarly obese, their transcript expression of ACC, PPARgamma, and FABP3 was similar to that of lean animals, indicating altered cardiac energy metabolism. Indeed, blunted tachycardia and an amplified inotropic response to hypotension characterized cardiac function in obese NR offspring. The results suggest that maternal NR during early organogenesis can precipitate an altered myocardial response to hypotension and increased myocardial lipid deposition in the adult offspring after adolescent-onset obesity, potentially rendering these individuals more at risk of early heart failure as they age. Journal Article AJP: Regulatory, Integrative and Comparative Physiology 296 5 R1455 R1463 0363-6119 1522-1490 31 5 2009 2009-05-31 10.1152/ajpregu.91019.2008 http://ajpregu.physiology.org/cgi/pmidlookup?view=long&amp;pmid=19244582 COLLEGE NANME Medical School COLLEGE CODE MEDS Swansea University 2011-10-01T00:00:00.0000000 2012-07-20T11:50:08.1482378 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine L. L. Y Chan 1 S. P Sebert 2 M. A Hyatt 3 T Stephenson 4 H Budge 5 M. E Symonds 6 D. S Gardner 7 Melanie Healy 8
title Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
spellingShingle Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
Melanie Healy
title_short Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
title_full Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
title_fullStr Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
title_full_unstemmed Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
title_sort Effect of maternal nutrient restriction from early to midgestation on cardiac function and metabolism after adolescent-onset obesity
author_id_str_mv 4654b4128fb21d68f98e2abc8538b45a
author_id_fullname_str_mv 4654b4128fb21d68f98e2abc8538b45a_***_Melanie Healy
author Melanie Healy
author2 L. L. Y Chan
S. P Sebert
M. A Hyatt
T Stephenson
H Budge
M. E Symonds
D. S Gardner
Melanie Healy
format Journal article
container_title AJP: Regulatory, Integrative and Comparative Physiology
container_volume 296
container_issue 5
container_start_page R1455
publishDate 2009
institution Swansea University
issn 0363-6119
1522-1490
doi_str_mv 10.1152/ajpregu.91019.2008
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://ajpregu.physiology.org/cgi/pmidlookup?view=long&amp;pmid=19244582
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description Maternal nutrient restriction (NR) from early to midgestation has marked effects on endocrine sensitivity and organ function of the resulting offspring. We hypothesized that early NR may reset the expression profile of genes central to myocardial energy metabolism, influencing ectopic lipid deposition and cardiac function in the obese adult offspring. NR offspring were exposed to an "obesogenic" environment, and their cardiac function and molecular indexes of myocardial energy metabolism were assessed to explore the hypothesis that an obese individual's risk of heart disease may be modified after maternal NR. Pregnant sheep were fed 100% (control) or 50% (NR) energy requirement from days 30 to 80 of gestation and 100% energy requirement thereafter. At weaning, offspring were exposed to an obesogenic environment or remained lean. At approximately 1 yr of age, the hemodynamic response of these offspring to hypotension, together with left ventricular expression profiles of fatty acid-binding protein 3 (FABP3), peroxisome proliferator-activated receptor-gamma (PPARgamma) and its coactivator (PGC)-1alpha, acetyl-CoA carboxylase (ACC), AMP-activated protein kinase (AMPK)-alpha(2), and voltage-dependent anion channel 1 (VDAC1), was determined. Obesity produced left ventricular hypertrophy in all animals, with increased ectopic (myocardial) lipid in NR offspring. Obesity per se significantly reduced myocardial transcript expression of PGC-1alpha, AMPKalpha(2), VDAC1, and ACC and increased expression of PPARgamma and FABP3. However, although NR animals were similarly obese, their transcript expression of ACC, PPARgamma, and FABP3 was similar to that of lean animals, indicating altered cardiac energy metabolism. Indeed, blunted tachycardia and an amplified inotropic response to hypotension characterized cardiac function in obese NR offspring. The results suggest that maternal NR during early organogenesis can precipitate an altered myocardial response to hypotension and increased myocardial lipid deposition in the adult offspring after adolescent-onset obesity, potentially rendering these individuals more at risk of early heart failure as they age.
published_date 2009-05-31T18:23:13Z
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