The aim of the present study was to evaluate the placental expression of glucose transporters GLUT‐1, GLUT‐3, GLUT‐8 and GLUT‐12 in term pregnancies complicated by well‐controlled gestational (GDM) and type 1 pregestational diabetes mellitus (PGDM).
A total of 103 placental samples were obtained from patients diagnosed with GDM ( n = 60), PGDM ( n = 20) and a non‐diabetic control group ( n = 23). Computer‐assisted quantitative morphometry of stained placental sections was performed to determine the expression of selected GLUT proteins.
Immunohistochemical techniques used for the identification of GLUT‐1, GLUT‐3, GLUT‐8 and GLUT‐12 revealed the presence of all glucose transporters in the placental tissue. Morphometric evaluation performed for the vascular density‐matched placental samples demonstrated a significant increase in the expression of GLUT‐1 protein in patients with PGDM as compared to GDM and control groups ( P < 0.05). With regard to the expression of the other GLUT isoforms, no statistically significant differences were observed between patients from the diabetic and control populations. Positive correlations between fetal birthweight and the expression of GLUT‐1 protein in the PGDM group (rho = 0.463, P < 0.05) and GLUT‐12 in the control group (rho = 0.481, P < 0.05) were noted.
In pregnancies complicated by gestational/pregestational diabetes mellitus, alterations in the placental GLUT expression might lead to an increased glucose flux into the fetal circulation, and thus fetal macrosomia. Study results demonstrated significantly increased GLUT‐1 expression in patients with pregestational diabetes mellitus as compared to women affected by GDM and healthy controls. In addition, in the former group of patients, GLUT‐1 expression was positively correlated with the fetal birthweight. With regard to GLUT‐3, 8 and 12 proteins, no significant differences were observed between diabetic and normoglycemic pregnancies. Increased expression of GLUT‐1 among women with type 1 pregestational diabetes mellitus might contribute to a higher rate of macrosomic fetuses in this population.