In utero undernutrition programs skeletal and cardiac muscle metabolism
In utero undernutrition is associated with increased risk for insulin resistance, obesity, and cardiovascular disease during adult life. A common phenotype associated with low birth weight is reduced skeletal muscle mass. Given the central role of skeletal muscle in whole body metabolism, alteration...
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doaj-44559541dbad4b6b838eca321505463d2020-11-24T23:12:09ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2016-01-01610.3389/fphys.2015.00401171634In utero undernutrition programs skeletal and cardiac muscle metabolismBrittany eBeauchamp0Mary-Ellen eHarper1University of OttawaUniversity of OttawaIn utero undernutrition is associated with increased risk for insulin resistance, obesity, and cardiovascular disease during adult life. A common phenotype associated with low birth weight is reduced skeletal muscle mass. Given the central role of skeletal muscle in whole body metabolism, alterations in its mass as well as its metabolic characteristics may contribute to disease risk. This review highlights the metabolic alterations in cardiac and skeletal muscle associated with in utero undernutrition and low birth weight. These tissues have high metabolic demands and are known to be sites of major metabolic dysfunction in obesity, type 2 diabetes, and cardiovascular disease. Recent research demonstrates that mitochondrial energetics are decreased in skeletal and cardiac muscles of adult offspring from undernourished mothers. These effects apparently lead to the development of a thrifty phenotype, which may represent overall a compensatory mechanism programmed in utero to handle times of limited nutrient availability. However, in an environment characterized by food abundance, the effects are maladaptive and increase adulthood risks of metabolic disease.http://journal.frontiersin.org/Journal/10.3389/fphys.2015.00401/fullMitochondriaOxidative Phosphorylationepigeneticsintrauterine growth restrictionUncouplingmetabolic programming |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Brittany eBeauchamp Mary-Ellen eHarper |
spellingShingle |
Brittany eBeauchamp Mary-Ellen eHarper In utero undernutrition programs skeletal and cardiac muscle metabolism Frontiers in Physiology Mitochondria Oxidative Phosphorylation epigenetics intrauterine growth restriction Uncoupling metabolic programming |
author_facet |
Brittany eBeauchamp Mary-Ellen eHarper |
author_sort |
Brittany eBeauchamp |
title |
In utero undernutrition programs skeletal and cardiac muscle metabolism |
title_short |
In utero undernutrition programs skeletal and cardiac muscle metabolism |
title_full |
In utero undernutrition programs skeletal and cardiac muscle metabolism |
title_fullStr |
In utero undernutrition programs skeletal and cardiac muscle metabolism |
title_full_unstemmed |
In utero undernutrition programs skeletal and cardiac muscle metabolism |
title_sort |
in utero undernutrition programs skeletal and cardiac muscle metabolism |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Physiology |
issn |
1664-042X |
publishDate |
2016-01-01 |
description |
In utero undernutrition is associated with increased risk for insulin resistance, obesity, and cardiovascular disease during adult life. A common phenotype associated with low birth weight is reduced skeletal muscle mass. Given the central role of skeletal muscle in whole body metabolism, alterations in its mass as well as its metabolic characteristics may contribute to disease risk. This review highlights the metabolic alterations in cardiac and skeletal muscle associated with in utero undernutrition and low birth weight. These tissues have high metabolic demands and are known to be sites of major metabolic dysfunction in obesity, type 2 diabetes, and cardiovascular disease. Recent research demonstrates that mitochondrial energetics are decreased in skeletal and cardiac muscles of adult offspring from undernourished mothers. These effects apparently lead to the development of a thrifty phenotype, which may represent overall a compensatory mechanism programmed in utero to handle times of limited nutrient availability. However, in an environment characterized by food abundance, the effects are maladaptive and increase adulthood risks of metabolic disease. |
topic |
Mitochondria Oxidative Phosphorylation epigenetics intrauterine growth restriction Uncoupling metabolic programming |
url |
http://journal.frontiersin.org/Journal/10.3389/fphys.2015.00401/full |
work_keys_str_mv |
AT brittanyebeauchamp inuteroundernutritionprogramsskeletalandcardiacmusclemetabolism AT maryelleneharper inuteroundernutritionprogramsskeletalandcardiacmusclemetabolism |
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