Fetomaternal Expression of Glucose Transporters (GLUTs)-Biochemical, Cellular and Clinical Aspects

Several types of specialized glucose transporters (GLUTs) provide constant glucose transport from the maternal circulation to the developing fetus through the placental barrier from the early stages of pregnancy. GLUT1 is a prominent protein isoform that regulates placental glucose transfer via glucose-facilitated diffusion. The GLUT1 membrane protein density and permeability of the syncytial basal membrane (BM) are the main factors limiting the rate of glucose diffusion in the fetomaternal compartment in physiological conditions. Besides GLUT1, the GLUT3 and GLUT4 isoforms are widely expressed across the human placenta. Numerous medical conditions and molecules, such as hormones, adipokines, and xenobiotics, alter the GLUT's mRNA and protein expression. Diabetes upregulates the BM GLUT's density and promotes fetomaternal glucose transport, leading to excessive fetal growth. However, most studies have found no between-group differences in GLUTs' placental expression in macrosomic and normal control pregnancies. The fetomaternal GLUTs expression may also be influenced by several other conditions, such as chronic hypoxia, preeclampsia, and intrahepatic cholestasis of pregnancy.

Automated summary

Several types of specialized glucose transporters (GLUTs) facilitate continuous glucose transport from the maternal circulation to the developing fetus through the placenta. GLUT1, GLUT3, and GLUT4 are the main isoforms expressed across the human placenta. Diabetes increases GLUT1 expression and promotes fetal glucose transport, leading to excessive fetal growth. Other conditions such as chronic hypoxia, preeclampsia, and intrahepatic cholestasis of pregnancy may also influence the expression of fetomaternal glucose transporters.