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Glucose Transporter Proteins (GLUT) in Human Endometrium: Expression, Regulation, and Function throughout the Menstrual Cycle and in Early Pregnancy

Departments of Gynecological Endocrinology and Reproductive Medicine (M.v.W., S.U., T.S.) and Obstetrics and Gynecology (U.H.), University of Heidelberg, 69115 Heidelberg; and Department of Obstetrics and Gynecology (R.S.), 83209 Prien am Chiemsee, Germany

Address all correspondence and requests for reprints to: Michael von Wolff, M.D., Universitaetsfrauenklinik Heidelberg, Abteilung Endokrinologie und Fertilitaetsstoerungen, Vossstrabe 9, 69115 Heidelberg, Germany. E-mail: michael.von.wolff{at}med.uni-heidelberg.de.

An adequate endometrial glucose metabolism, mediated by facilitative glucose transporter molecules (GLUT), is an essential part of endometrial differentiation and decidualization to provide a nutritional and receptive milieu. In human endometrium, only the GLUT1 and GLUT3 isoforms are expressed, whereas glucose transporters, involved in insulin-dependent glucose uptake (GLUT2, GLUT4, GLUT8), could not be detected. Messenger RNA expression, analyzed by RNase protection assay, of both isoforms increased in total endometrium throughout the secretory phase and in decidua. Analysis of mRNA expression in isolated epithelial cells, stromal cells, and CD45 positive leukocytes revealed that increase of GLUT1 expression was due to increasing stromal expression, whereas increase of GLUT3 was due to its expression in CD45-positive immune cells. In vitro, GLUT1 and GLUT3 were not directly regulated by 17ß-estradiol, progesterone, or IL-1ß, IL-6, and leukemia inhibitory factor, but GLUT1 mRNA increased progressively in stromal cells, decidualized in vitro. Inhibition of glucose transporters by cytochalasin B reduced stromal glucose uptake and stromal decidualization. In idiopathic infertile patients, GLUT1 expression in midsecretory endometrium was suppressed. The suppression was caused by reduced stromal expression. Our results suggest stromal GLUT to play a role in the regulation of endometrial function and be compromised in the preparation of the endometrium for the implanting embryo.

Abbreviations: GAPDH, Glyceraldehyde-3-phosphate dehydrogenase; PRL, prolactin; RPA, RNase protection assay.

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