Show simple item record

dc.contributor.authorYates, DTen_US
dc.contributor.authorMacko, ARen_US
dc.contributor.authorNearing, Men_US
dc.contributor.authorChen, Xen_US
dc.contributor.authorRhoads, RPen_US
dc.contributor.authorLimesand, SWen_US
dc.identifier.citationD. T. Yates, A. R. Macko, M. Nearing, X. Chen, R. P. Rhoads, and S. W. Limesand, “Developmental Programming in Response to Intrauterine Growth Restriction Impairs Myoblast Function and Skeletal Muscle Metabolism,” Journal of Pregnancy, vol. 2012, Article ID 631038, 10 pages, 2012. doi:10.1155/2012/631038
dc.description.abstractFetal adaptations to placental insufficiency alter postnatal metabolic homeostasis in skeletal muscle by reducing glucose oxidation rates, impairing insulin action, and lowering the proportion of oxidative fibers. In animal models of intrauterine growth restriction (IUGR), skeletal muscle fibers have less myonuclei at birth. This means that myoblasts, the sole source for myonuclei accumulation in fibers, are compromised. Fetal hypoglycemia and hypoxemia are complications that result from placental insufficiency. Hypoxemia elevates circulating catecholamines, and chronic hypercatecholaminemia has been shown to reduce fetal muscle development and growth. We have found evidence for adaptations in adrenergic receptor expression profiles in myoblasts and skeletal muscle of IUGR sheep fetuses with placental insufficiency. The relationship of β-adrenergic receptors shifts in IUGR fetuses because Adrβ2 expression levels decline and Adrβ1 expression levels are unaffected in myofibers and increased in myoblasts. This adaptive response would suppress insulin signaling, myoblast incorporation, fiber hypertrophy, and glucose oxidation. Furthermore, this β-adrenergic receptor expression profile persists for at least the first month in IUGR lambs and lowers their fatty acid mobilization. Developmental programming of skeletal muscle adrenergic receptors partially explains metabolic and endocrine differences in IUGR offspring, and the impact on metabolism may result in differential nutrient utilization.en_US
dc.format.extent631038 - ? page(s)en_US
dc.rightsCreative Commons Attribution 3.0 Unported (CC BY 3.0)*
dc.subjectAdaptation, Physiologicalen_US
dc.subjectFetal Developmenten_US
dc.subjectFetal Growth Retardationen_US
dc.subjectFetal Hypoxiaen_US
dc.subjectMuscle Developmenten_US
dc.subjectMuscle, Skeletalen_US
dc.subjectMyoblasts, Skeletalen_US
dc.subjectPlacental Insufficiencyen_US
dc.subjectPrenatal Exposure Delayed Effectsen_US
dc.titleDevelopmental programming in response to intrauterine growth restriction impairs myoblast function and skeletal muscle metabolism.en_US
dc.typeArticle - Refereed
dc.description.versionPublished (Publication status)en_US
dc.rights.holderCopyright © 2012 D. T. Yates et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.title.serialJ Pregnancyen_US
pubs.organisational-group/Virginia Tech
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/Animal and Poultry Sciences
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/CALS T&R Faculty
pubs.organisational-group/Virginia Tech/All T&R Faculty
pubs.organisational-group/Virginia Tech/Faculty of Health Sciences

Files in this item


This item appears in the following Collection(s)

Show simple item record

Creative Commons Attribution 3.0 Unported (CC BY 3.0)
License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)