developmental programming in response to intrauterine growth restriction impairs myoblast function and skeletal muscle metabolism发展规划以应对宫内生长受限影响骨骼肌成肌细胞功能和新陈代谢.pdfVIP

Hindawi Publishing Corporation Journal of Pregnancy Volume 2012, Article ID 631038, 10 pages doi:10.1155/2012/631038 Review Article Developmental Programming in Response to Intrauterine Growth Restriction Impairs Myoblast Function and Skeletal Muscle Metabolism D. T. Yates,1 A. R. Macko,1 M. Nearing,1 X. Chen,1 R. P. Rhoads,2 and S. W. Limesand1, 3 1 Department of Animal Sciences, The University of Arizona, Tucson, AZ 85721-0038, USA 2 Department of Animal and Poultry Sciences, Virginia Tech, Blacksburg, VA 24061, USA 3 Agricultural Research Complex, Department of Animal Sciences, The University of Arizona, 1650 E. Limberlost Dr., Tucson, AZ 85719, USA Correspondence should be addressed to S. W. Limesand, limesand@ Received 1 April 2012; Accepted 25 May 2012 Academic Editor: Timothy Regnault Copyright © 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. Fetal 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 e