title: Glucose transporter expression in eutopic endometrial tissue and ectopic endometriotic lesions.
abstract: Endometriosis is an extremely prevalent disorder characterized by the growth of endometrial tissue at ectopic locations. Glycolysis is an energy-producing mechanism that occurs in almost all cells and requires an adequate uptake of glucose mediated by glucose transporter (GLUT) proteins. At present, however, very little is known about their expression in either the endometrium or the endometriotic lesions. The objective of this study was to examine the expression of SLC2A genes in the endometrium of women with and without endometriosis and in the matching ectopic tissue, and to confirm the presence of the GLUT proteins in ectopic lesions. There was a significantly higher expression of SLC2A3 and a significantly lower expression of SLC2A4 in women with endometriosis compared with those without. In women with endometriosis, the ectopic expression of SLC2A3, SLC2A4 and SLC2A5 was significantly higher than that observed in the matching eutopic tissue. GLUT1 protein expression was present in both epithelial and stromal cells and GLUT3 was confined to CD45-positive leukocytes. GLUT4 expression was strong in both ectopic epithelial and stromal cells and localized to the cellular membrane in epithelial cells. These results show that GLUT expression is altered between eutopic and ectopic tissue and between women with and without endometriosis, and that GLUT4 may represent a significant entry route for glucose into the endometriotic epithelial cells. The inducible nature of GLUT4 and its limited cellular expression may make GLUT4 an attractive target for non-hormone-based treatments of endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, Inselspital, Berne University Hospital, Effingerstrasse 102, Berne CH-3010, Switzerland Department of Clinical Research, University of Bern, Murtenstrasse 35, Bern CH-3010, Switzerland.
authors.forename: Brett
authors.initials: B
authors.lastname: McKinnon
authors.forename: Dominic
authors.initials: D
authors.lastname: Bertschi
authors.forename: Carlos
authors.initials: C
authors.lastname: Wotzkow
authors.forename: Nick A
authors.initials: NA
authors.lastname: Bersinger
authors.forename: Jakob
authors.initials: J
authors.lastname: Evers
authors.forename: Michael D
authors.initials: MD
authors.lastname: Mueller
mesh_terms: D000328:Adult; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002828:Choristoma / Q000235:genetics* / Q000473:pathology; D004715:Endometriosis / Q000235:genetics* / Q000473:pathology; D004717:Endometrium / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics* / Q000378:metabolism; D006728:Hormones / Q000494:pharmacology; D006801:Humans; D021381:Protein Transport / Q000187:drug effects / Q000235:genetics
chemical_list: D051246:Glucose Transport Proteins, Facilitative; D006728:Hormones
keywords: GLUT4; SLC2A; endometriosis; endometrium; glucose