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Expression of Glucose Transporter Proteins (GLUTs) in Human Placental Tissue after Normal vs. Diabetic Pregnancy
Author(s) -
Szukiewicz Dariusz,
Stanirowski Pawel Jan,
Pyzlak Michal,
Abdalla Nabil,
Sawicki Wlodzimierz,
Cendrowski Krzysztof
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.976.12
Subject(s) - glucose transporter , medicine , diabetes mellitus , endocrinology , insulin , gestational diabetes , placenta , pregnancy , immunohistochemistry , gestation , biology , fetus , genetics
Altered expression of GLUTs in diabetic placenta has been suggested recently by independent authors, including the role of insulin therapy as a possible modulatory factor. In this study we examined comparatively the expression of GLUTs (GLUT‐1, GLUT‐4, and GLUT‐9) in the placental tissue obtained after normal healthy and diabetic pregnancies. Additionally, the effect of insulin therapy on the expression of selected GLUTs isoforms was analyzed. Placental samples derived from healthy gravidas after normal term pregnancies (N = 25) and obtained after diabetic pregnancies, including diet‐controlled gestational diabetes mellitus (GDMG1; N = 16), insulin‐controlled GDM (GDMG2; N = 6), and pre‐gestational DM (PGDM; N = 6). To visualize GLUT‐1, GLUT‐4, and GLUT‐9, standard immunohistochemical procedures were used with the respective anti‐GLUT antibodies. Thereafter, computer‐assisted quantitative morphometry was performed to identify immunostained GLUTs in 5‐μm paraffin‐embedded sections of the placental specimens, and the final results were adjusted for the mean microvascular density with the permitted margin of error not exceeding ± 5 %. Morphometric evaluation revealed a significant increase (p < 0.05) in the mean expression of GLUT‐4 and GLUT‐9 in insulin‐dependent diabetes (GDMG2 + PGDM) as compared to both, the control and GDMG1 groups. A significant increase in the mean GLUT‐1 expression was observed only in placental specimens obtained from PGDM group (p < 0.05). The differences in GLUTs expression between GDMG1 group and the healthy controls did not reach statistical significance. In conclusion, our results have confirmed the presence of GLUT‐1, GLUT‐4 and GLUT‐9 proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. Interestingly, insulin therapy may significantly increase placental expression of GLUT‐4 and GLUT‐9 isoforms, and partially GLUT‐1, in diabetic gravidas classified as GDMG2 and PGDM. Support or Funding Information WUM grant: 2WA/PM23D/14