[HTML][HTML] Impact of pre-gestational and gestational diabetes mellitus on the expression of glucose transporters GLUT-1, GLUT-4 and GLUT-9 in human term placenta

PJ Stanirowski, D Szukiewicz, M Pyzlak, N Abdalla… - Endocrine, 2017 - Springer
PJ Stanirowski, D Szukiewicz, M Pyzlak, N Abdalla, W Sawicki, K Cendrowski
Endocrine, 2017Springer
Purpose Various studies in placental tissue suggest that diabetes mellitus alters the
expression of glucose transporter (GLUT) proteins, with insulin therapy being a possible
modulatory factor. The aim of the present study was quantitative evaluation of the expression
of glucose transporters (GLUT-1, GLUT-4, GLUT-9) in the placenta of women in both,
uncomplicated and diabetic pregnancy. Additionally, the effect of insulin therapy on the
expression of selected glucose transporter isoforms was analyzed. Methods Term placental …
Purpose
Various studies in placental tissue suggest that diabetes mellitus alters the expression of glucose transporter (GLUT) proteins, with insulin therapy being a possible modulatory factor. The aim of the present study was quantitative evaluation of the expression of glucose transporters (GLUT-1, GLUT-4, GLUT-9) in the placenta of women in both, uncomplicated and diabetic pregnancy. Additionally, the effect of insulin therapy on the expression of selected glucose transporter isoforms was analyzed.
Methods
Term placental samples were obtained from healthy control (n = 25) and diabetic pregnancies, including diet-controlled gestational diabetes mellitus (GDMG1) (n = 16), insulin-controlled gestational diabetes mellitus (GDMG2) (n = 6), and pre-gestational diabetes mellitus (PGDM) (n = 6). Computer-assisted quantitative morphometry of stained placental sections was performed to determine the expression of selected glucose transporter proteins.
Results
Morphometric analysis revealed a significant increase in the expression of GLUT-4 and GLUT-9 in insulin-dependent diabetic women (GDMG2 + PGDM) as compared to both, control and GDMG1 groups (p < .05). Significantly increased GLUT-1 expression was observed only in placental specimens from patients with PGDM (p < .05). No statistically significant differences in GLUT expression were found between GDMG1 patients and healthy controls.
Conclusions
The results of the study confirmed the presence of GLUT-1, GLUT-4 and GLUT-9 proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin therapy may increase placental expression of GLUT-4 and GLUT-9, and partially GLUT-1, in women with GDMG2/PGDM.
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