Expression of placental glucose transporter proteins in pregnancies complicated by fetal growth disorders

Adv Protein Chem Struct Biol. 2021:123:95-131. doi: 10.1016/bs.apcsb.2019.12.003. Epub 2020 Jan 22.

Abstract

During pregnancy fetal growth disorders, including fetal macrosomia and fetal growth restriction (FGR) are associated with numerous maternal-fetal complications, as well as due to the adverse effect of the intrauterine environment lead to an increased morbidity in adult life. Accumulating evidence suggests that occurrence of fetal macrosomia or FGR, may be associated with alterations in the transfer of nutrients across the placenta, in particular of glucose. The placental expression and activity of specific GLUT transporters are the main regulatory factors in the process of maternal-fetal glucose exchange. This review article summarizes the results of previous studies on the expression of GLUT transporters in the placenta, concentrating on human pregnancies complicated by intrauterine fetal growth disorders. Characteristics of each transporter protein found in the placenta is presented, alterations in the location and expression of GLUT isoforms observed in individual placental compartments are described, and the factors regulating the expression of selected GLUT proteins are examined. Based on the above data, the potential function of each GLUT isoform in the maternal-fetal glucose transfer is determined. Further on, a detailed analysis of changes in the expression of glucose transporters in pregnancies complicated by fetal growth disorders is given, and significance of these modifications for the pathogenesis of fetal macrosomia and FGR is discussed. In the final part novel interventional approaches that might reduce the risk associated with abnormalities of intrauterine fetal growth through modifications of placental GLUT-mediated glucose transfer are explored.

Keywords: Fetal growth restriction; Fetal macrosomia; GLUT; Glucose transporter; Placenta.

Publication types

  • Review

MeSH terms

  • Female
  • Fetal Growth Retardation / metabolism*
  • Fetal Growth Retardation / pathology
  • Gene Expression Regulation, Developmental*
  • Glucose Transport Proteins, Facilitative / biosynthesis*
  • Humans
  • Placenta / metabolism*
  • Placenta / pathology
  • Pregnancy

Substances

  • Glucose Transport Proteins, Facilitative