Article

Endocrine

, Volume 19, Issue 1, pp 13-22

Placental glucose transfer and fetal growth

  • Marc U. BaumannAffiliated withDepartment of Obstetrics, Gynecology and Women’s Health, University of Medicine and Dentistry of New Jersey, New Jersey Medical School
  • , Sylvie DebordeAffiliated withDepartment of Obstetrics, Gynecology and Women’s Health, University of Medicine and Dentistry of New Jersey, New Jersey Medical School
  • , Nicholas P. IllsleyAffiliated withDepartment of Obstetrics, Gynecology and Women’s Health, University of Medicine and Dentistry of New Jersey, New Jersey Medical School Email author 

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Abstract

One of the primary regulators of maternofetal glucose transfer is the density of glucose transporter proteins in the placenta. These transporters, members of the GLUT gene family of facilitated-diffusion transporters, are embedded in the microvillous (maternal-facing) and basal (fetal-facing) membranes of the syncytiotrophoblast, the main placental barrier layer. Eight members of this family have been described in human placental tissue, but only GLUT1 protein has been identified in the syncytium, where its distribution is asymmetric. The microvillous membrane contains markedly more transporter than the basal, and, as a result, the basal membrane acts as the rate-limiting step in transplacental glucose transport; thus, changes in the density of basal membrane GLUT1 will have a significant impact on transplacental glucose flux. What little is known about syncytial GLUT1 expression is restricted to factors associated with fetoplacental growth and metabolism; GLUT is inversely regulated by glucose concentration and basal membrane GLUT1 is positively regulated by insulin-like growth factor I, placental growth hormone, and hypoxia. In vivo, basal membrane GLUT1 is upregulated over gestation, increased in diabetic pregnancy, and decreased in chronic hypoxia, while microvillous membrane GLUT1 is unaffected. The contrast between in vitro and in vivo regulation and the specific changes in GLUT1 distribution suggest more complex regulatory interactions than those yet described.

Key Words

Glucose transfer syncytiotrophoblast placenta hypoxia rate-limiting step GLUT