Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 435, Issue C, Pages 69-77Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2016.03.017
Keywords
Amino acids; Muscle protein synthesis; Myofiber; Myoblast; Myogenesis; Developmental programming
Categories
Funding
- NIH [R0 HD079404, T32 HD007186, K12 HD068372, R0 DK088139, UL1TR001082]
- University of Colorado Center for Women's Health Research
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Intrauterine growth restriction (IUGR) caused by placental insufficiency is one of the most common and complex problems in perinatology, with no known cure. In pregnancies affected by placental insufficiency, a poorly functioning placenta restricts nutrient supply to the fetus and prevents normal fetal growth. Among other significant deficits in organ development, the IUGR fetus characteristically has less lean body and skeletal muscle mass than their appropriately-grown counterparts. Reduced skeletal muscle growth is not fully compensated after birth, as individuals who were born small for gestational age (SGA) from IUGR have persistent reductions in muscle mass and strength into adulthood. The consequences of restricted muscle growth and accelerated postnatal catch-up growth in the form of adiposity may contribute to the increased later life risk for visceral adiposity, peripheral insulin resistance, diabetes, and cardiovascular disease in individuals who were formerly IUGR. This review will discuss how an insufficient placenta results in impaired fetal skeletal muscle growth and how lifelong reductions in muscle mass might contribute to increased metabolic disease risk in this vulnerable population. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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