Brown Laura D, Hay William W
Department of Pediatrics, University of Colorado School of Medicine, Anschutz Medical Campus F441, Perinatal Research Center, 13243 East 23rd Avenue, Aurora, CO 80045, United States.
Mol Cell Endocrinol. 2016 Nov 5;435:69-77. doi: 10.1016/j.mce.2016.03.017. Epub 2016 Mar 16.
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.
胎盘功能不全导致的胎儿宫内生长受限(IUGR)是围产医学中最常见且复杂的问题之一,目前尚无治愈方法。在受胎盘功能不全影响的妊娠中,功能不佳的胎盘会限制对胎儿的营养供应,阻碍胎儿正常生长。在器官发育的其他显著缺陷中,IUGR胎儿的瘦体重和骨骼肌量通常比生长正常的胎儿少。骨骼肌生长减少在出生后无法完全代偿,因为因IUGR而出生时小于胎龄(SGA)的个体,其肌肉量和力量在成年后仍持续降低。肌肉生长受限以及以肥胖形式出现的加速出生后“追赶”生长,可能会导致曾患IUGR的个体日后患内脏肥胖、外周胰岛素抵抗、糖尿病和心血管疾病的风险增加。本综述将讨论胎盘功能不全会如何导致胎儿骨骼肌生长受损,以及肌肉量的终身减少可能如何导致这一脆弱人群患代谢性疾病的风险增加。