Journal of diabetes investigation · 2021
Placental expression of glucose transporters GLUT-1, GLUT-3, GLUT-8 and GLUT-12 in pregnancies complicated by gestational and type 1 diabetes mellitus.
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Stanirowski Paweł Jan, Szukiewicz Dariusz, Majewska Agata, Wątroba Mateusz, Pyzlak Michał, Bomba-Opoń Dorota, Wielgoś Mirosław
Аннотация
AIMS/INTRODUCTION: 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).
MATERIALS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: In term pregnancies complicated by well-controlled GDM/PGDM, expression of transporters GLUT-3, GLUT-8 and GLUT-12 in the placenta remains unaffected. Increased expression of GLUT-1 among women with type 1 PGDM might contribute to a higher rate of macrosomic fetuses in this population.
MATERIALS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: In term pregnancies complicated by well-controlled GDM/PGDM, expression of transporters GLUT-3, GLUT-8 and GLUT-12 in the placenta remains unaffected. Increased expression of GLUT-1 among women with type 1 PGDM might contribute to a higher rate of macrosomic fetuses in this population.