Interaction between maternal obesity and post-natal over-nutrition on skeletal muscle metabolism

Simar, D; Chen, H; Lambert, K; Mercier, J; Morris, MJ

Interaction between maternal obesity and post-natal over-nutrition on skeletal muscle metabolism

Simar, D Chen, H

Lambert, K Mercier, J Morris, MJ

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Publication Type:: Journal Article
Citation:: Nutrition, Metabolism and Cardiovascular Diseases, 2012, 22 (3), pp. 269 - 276
Issue Date:: 2012-03-01

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Field	Value	Language
dc.contributor.author	Simar, D	en_US
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.contributor.author	Lambert, K	en_US
dc.contributor.author	Mercier, J	en_US
dc.contributor.author	Morris, MJ	en_US
dc.date.available	2010-11-21	en_US
dc.date.issued	2012-03-01	en_US
dc.identifier.citation	Nutrition, Metabolism and Cardiovascular Diseases, 2012, 22 (3), pp. 269 - 276	en_US
dc.identifier.issn	0939-4753	en_US
dc.identifier.uri	http://hdl.handle.net/10453/29483
dc.description.abstract	Background and aims: Maternal obesity and post-natal over-nutrition play an important role in programming glucose and lipid metabolism later in life. The aim of this study was to decipher the contributions of maternal obesity and post-natal over-nutrition on glucose and lipid metabolism in skeletal muscle. Method and results: Male offspring of Sprague Dawley rat mothers fed either chow or high fat diet (HFD) for 5 weeks prior to mating were subsequently fed either chow or HFD until 18 weeks of age. Collection of plasma and skeletal muscle was performed at weaning (20 days) and 18 weeks. At weaning, offspring from obese mothers showed increased body weight, plasma insulin and lactate concentrations associated with reduced skeletal muscle glucose transporter 4 (GLUT4) and increased monocarboxylate transporter 1 (MCT1) protein. In 18-week old offspring, post-weaning HFD further exacerbated the elevated body weight caused by maternal obesity. Surprisingly this additive effect on body weight was not reflected in plasma glucose, insulin, lactate and MCT1; these markers were only increased by post-weaning HFD consumption. However, an additive effect of maternal obesity and post-weaning HFD led to decreased muscle GLUT4 levels, as well as mRNA levels of carnitine palmitoyl transferase-1, myogenic differentiation protein and myogenin. Conclusion: Post-weaning HFD exerted an additive effect to that of maternal obesity on body weight and skeletal muscle markers of glucose and lipid metabolism but not on plasma glucose and insulin levels, suggesting that maternal obesity and post-natal over-nutrition impair skeletal muscle function via different mechanisms. © 2010 Elsevier B.V.	en_US
dc.relation.ispartof	Nutrition, Metabolism and Cardiovascular Diseases	en_US
dc.relation.isbasedon	10.1016/j.numecd.2010.11.007	en_US
dc.subject.classification	Cardiovascular System & Hematology	en_US
dc.subject.mesh	Muscle, Skeletal	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Rats	en_US
dc.subject.mesh	Rats, Sprague-Dawley	en_US
dc.subject.mesh	Prenatal Exposure Delayed Effects	en_US
dc.subject.mesh	Overnutrition	en_US
dc.subject.mesh	Obesity	en_US
dc.subject.mesh	Body Weight	en_US
dc.subject.mesh	Lactic Acid	en_US
dc.subject.mesh	Insulin	en_US
dc.subject.mesh	Monocarboxylic Acid Transporters	en_US
dc.subject.mesh	Symporters	en_US
dc.subject.mesh	Age Factors	en_US
dc.subject.mesh	Energy Metabolism	en_US
dc.subject.mesh	Weaning	en_US
dc.subject.mesh	Pregnancy	en_US
dc.subject.mesh	Female	en_US
dc.subject.mesh	Male	en_US
dc.subject.mesh	Glucose Transporter Type 4	en_US
dc.subject.mesh	Animal Nutritional Physiological Phenomena	en_US
dc.subject.mesh	Diet, High-Fat	en_US
dc.title	Interaction between maternal obesity and post-natal over-nutrition on skeletal muscle metabolism	en_US
dc.type	Journal Article
utslib.citation.volume	3	en_US
utslib.citation.volume	22	en_US
utslib.for	111103 Nutritional Physiology	en_US
utslib.for	1103 Clinical Sciences	en_US
utslib.for	11 Medical and Health Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	closed_access
pubs.issue	3	en_US
pubs.publication-status	Published	en_US
pubs.volume	22	en_US

Abstract:

Background and aims: Maternal obesity and post-natal over-nutrition play an important role in programming glucose and lipid metabolism later in life. The aim of this study was to decipher the contributions of maternal obesity and post-natal over-nutrition on glucose and lipid metabolism in skeletal muscle. Method and results: Male offspring of Sprague Dawley rat mothers fed either chow or high fat diet (HFD) for 5 weeks prior to mating were subsequently fed either chow or HFD until 18 weeks of age. Collection of plasma and skeletal muscle was performed at weaning (20 days) and 18 weeks. At weaning, offspring from obese mothers showed increased body weight, plasma insulin and lactate concentrations associated with reduced skeletal muscle glucose transporter 4 (GLUT4) and increased monocarboxylate transporter 1 (MCT1) protein. In 18-week old offspring, post-weaning HFD further exacerbated the elevated body weight caused by maternal obesity. Surprisingly this additive effect on body weight was not reflected in plasma glucose, insulin, lactate and MCT1; these markers were only increased by post-weaning HFD consumption. However, an additive effect of maternal obesity and post-weaning HFD led to decreased muscle GLUT4 levels, as well as mRNA levels of carnitine palmitoyl transferase-1, myogenic differentiation protein and myogenin. Conclusion: Post-weaning HFD exerted an additive effect to that of maternal obesity on body weight and skeletal muscle markers of glucose and lipid metabolism but not on plasma glucose and insulin levels, suggesting that maternal obesity and post-natal over-nutrition impair skeletal muscle function via different mechanisms. © 2010 Elsevier B.V.

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http://hdl.handle.net/10453/29483