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by qwen3.7-flash, 2026-08-22
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This study investigated glucose transporter 1 (GLUT-1) expression in the eutopic endometrium and various ectopic lesions from thirty-five women with deep-infiltrating endometriosis undergoing rectum resection. Immunohistochemical analysis revealed that GLUT-1 expression was stronger in the eutopic endometrium than in ectopic lesions, with significant upregulation observed in the late secretory phase of the menstrual cycle but absent during the proliferative phase. The findings indicate that GLUT-1 is expressed in endometriotic tissue and likely supports cellular metabolism under hypoxic conditions via HIF-1, VEGF, and EGFR pathways. This paper is centrally about endometriosis — specifically examining the molecular mechanisms of glucose metabolism in deep-infiltrating endometriosis and peritoneal lesions.
Abstract
Introduction: Glucose metabolism plays a important role in human tissues. In this respect, GLUT-1 seems to be one of the major factors in the complex hypoxia orchestra. Recent studies implicated that estrogen (E2) and progesterone (P) might play an important role in the regulation of glucose metabolism by regulation the glucose transporter (GLUT) expression. There is some evidence that defective glucose metabolism leads to infertility. Methods: 35 women with deep-infiltrating endometriosis who underwent rectum resection where included in the study. Immunohistochemistry (IHC) combined with a modified Remmele-Stegener-IHC-Score (0–3) was used. For data collection and statistical analysis (Mann-Whitney-Test) excel and SPSS were used. Results: In eutopic endometrium GLUT-1 expression was positive in epithelium cells as well as in stroma cells whereas in ectopic lesions mainly epithelium cells have been positive. Expression was stronger in endometrium than in ectopic lesions. No GLUT-1 expression was detectable in eutopic endometrium of the proliferative phase. In contrast, GLUT-1 expression was strong in the late secretory phase (p <, 001) in eutopic endometrium and in epithelium cells of DIE (p<0.004). In peritoneal lesions no cycle-dependend GLUT-1 expression could be detected. Conclusions: We did provide evidence that GLUT-1 is expressed in endometriosis. In addition, we support the hypothesis that the GLUT-1 expression is important for a sufficient glucose metabolism in eutopic endometrium and plays a role in endometrial differentiation in dependence on the menstrual cycle. GLUT-1 expression is regulated through the hypoxia inducible factor-1 (HIF-1) as well as the expression of vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR). Through the up regulation of these factors the cell tries to hold up its metabolism even under hypoxic conditions, known as survival pathway. GLUT-1 seems to be one of the factors, next to VEGF and EGFR, which might be necessary for the establishment of endometriosis.
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DOI: 10.1055/s-0031-1292727
Expression of GLUT-1 in human eutopic endometrium, in peritoneal endometriotic lesions, and in deep-infiltrating endometriosis
Introduction: Glucose metabolism plays a important role in human tissues. In this respect, GLUT-1 seems to be one of the major factors in the complex hypoxia orchestra. Recent studies implicated that estrogen (E2) and progesterone (P) might play an important role in the regulation of glucose metabolism by regulation the glucose transporter (GLUT) expression. There is some evidence that defective glucose metabolism leads to infertility. Methods: 35 women with deep-infiltrating endometriosis who underwent rectum resection where included in the study. Immunohistochemistry (IHC) combined with a modified Remmele-Stegener-IHC-Score (0–3) was used. For data collection and statistical analysis (Mann-Whitney-Test) excel and SPSS were used. Results: In eutopic endometrium GLUT-1 expression was positive in epithelium cells as well as in stroma cells whereas in ectopic lesions mainly epithelium cells have been positive. Expression was stronger in endometrium than in ectopic lesions. No GLUT-1 expression was detectable in eutopic endometrium of the proliferative phase. In contrast, GLUT-1 expression was strong in the late secretory phase (p <, 001) in eutopic endometrium and in epithelium cells of DIE (p<0.004). In peritoneal lesions no cycle-dependend GLUT-1 expression could be detected. Conclusions: We did provide evidence that GLUT-1 is expressed in endometriosis. In addition, we support the hypothesis that the GLUT-1 expression is important for a sufficient glucose metabolism in eutopic endometrium and plays a role in endometrial differentiation in dependence on the menstrual cycle. GLUT-1 expression is regulated through the hypoxia inducible factor-1 (HIF-1) as well as the expression of vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR). Through the up regulation of these factors the cell tries to hold up its metabolism even under hypoxic conditions, known as survival pathway. GLUT-1 seems to be one of the factors, next to VEGF and EGFR, which might be necessary for the establishment of endometriosis.
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