Department of Obstetrics, Gynecology and Oncology, II Faculty of Medicine, Medical University of Warsaw, Mazovian Bródno Hospital, Warsaw, Poland.
Department of General and Experimental Pathology with Centre for Preclinical Research and Technology (CEPT), II Faculty of Medicine, Medical University of Warsaw, Warsaw, Poland.
Can J Diabetes. 2018 Apr;42(2):209-217. doi: 10.1016/j.jcjd.2017.04.008. Epub 2017 Jun 2.
Gestational diabetes mellitus and pregestational diabetes mellitus constitute carbohydrate metabolism disorders, which, if not diagnosed and adequately treated, lead to serious and often life-threatening pregnancy complications. According to a recently formulated hypothesis, some diabetes-related complications, such as fetal macrosomia, may be the result of disturbances in the transplacental transport of nutrients-in particular, excessive maternal-fetal glucose transfer. Throughout pregnancy, glucose flux across the placenta is mediated by the group of facilitative glucose transporters (GLUT), the expression of which in different placental compartments is the precondition for effective glucose uptake from maternal blood and its subsequent transfer to the fetal circulation. In diabetes-complicated pregnancies, the location, expression and activity of glucose transporters are modified to an extent that results in alterations in the maternal-fetal glucose exchange, potentially leading to an excessive supply of energy substrates to the fetus. This paper reviews the literature on the expression and activity of glucose transporter proteins-GLUT-1, GLUT-3, GLUT-4, GLUT-8, GLUT-9 and GLUT-12-in the human placenta, with a special focus on diabetes-complicated pregnancy. The characteristics of transporters in conditions of maternal normoglycemia and modifications occurring in the diabetic placenta are summarized, and the factors responsible for the regulation of the expression of selected isoforms are described. Finally, the impact of alterations in the placental expression of the aforementioned members of the GLUT family on intrauterine fetal development in pregnancies complicated by diabetes mellitus is discussed.
妊娠期糖尿病和孕前糖尿病属于碳水化合物代谢紊乱，如果不能得到诊断和充分治疗，会导致严重且常常危及生命的妊娠并发症。根据最近提出的假说，一些与糖尿病相关的并发症，如胎儿巨大儿，可能是胎盘转运营养物质（尤其是母体-胎儿葡萄糖转运）紊乱的结果。在整个妊娠期间，葡萄糖通过胎盘的转运由一组易化葡萄糖转运体（GLUT）介导，不同胎盘隔室中这些转运体的表达是从母体血液有效摄取葡萄糖并随后将其转移到胎儿循环的前提。在糖尿病合并妊娠中，葡萄糖转运体的位置、表达和活性发生改变，导致母体-胎儿葡萄糖交换发生改变，可能导致胎儿能量底物供应过多。本文综述了人类胎盘葡萄糖转运蛋白（GLUT-1、GLUT-3、GLUT-4、GLUT-8、GLUT-9 和 GLUT-12）的表达和活性的文献，特别关注糖尿病合并妊娠。总结了在母体血糖正常和糖尿病胎盘情况下转运体的特征，以及负责调节某些同工型表达的因素。最后，讨论了 GLUT 家族上述成员在胎盘表达改变对糖尿病合并妊娠中宫内胎儿发育的影响。
