Gatford Kathryn L, Simmons Rebecca A
Robinson Institute, and School of Paediatrics and Reproductive Health, University of Adelaide, SA, Australia, USA.
Clin Obstet Gynecol. 2013 Sep;56(3):520-8. doi: 10.1097/GRF.0b013e31829e5b29.
Intrauterine growth restriction (IUGR) impairs insulin secretion in humans and in animal models of IUGR. Several underlying mechanisms have been implicated, including decreased expression of molecular regulators of β-cell mass and function, in some cases shown to be due to epigenetic changes initiated by an adverse fetal environment. Alterations in cell cycle progression contribute to loss of β-cell mass, whereas decreased islet vascularity and mitochondrial dysfunction impair β-cell function in IUGR rodents. Animal models of IUGR sharing similar insulin secretion outcomes as the IUGR human are allowing underlying mechanisms to be identified. This review will focus on models of uteroplacental insufficiency.
宫内生长受限（IUGR）会损害人类以及IUGR动物模型中的胰岛素分泌。已经涉及到几种潜在机制，包括β细胞量和功能的分子调节因子表达降低，在某些情况下表明这是由不良胎儿环境引发的表观遗传变化所致。细胞周期进程的改变导致β细胞量减少，而胰岛血管生成减少和线粒体功能障碍会损害IUGR啮齿动物的β细胞功能。与IUGR人类具有相似胰岛素分泌结果的IUGR动物模型有助于确定潜在机制。本综述将聚焦于子宫胎盘功能不全模型。
