P-343 Metformin reduces endometrial implants and improves fertility in a mouse model of endometriosis

Abstract Study question Could endometriosis-associated infertility be mitigated by metformin? Summary answer Metformin treatment restored fertility to control rates in endometriosis-induced mice that present lower fertility. Endometrial implants presented a reduction in size with metformin treatment. What is known already Endometriosis is an inflammatory disease characterized by estrogen-dependent ectopic growth of endometrium causing pain and infertility. Hormone-based medication prescribed need to be interrupted when women intend to conceive. Corroborating observations in women, endometriosis decreases oocyte quality and pregnancy success in rodents. Thus, animal models of endometriosis constitute a valuable tool to elucidate the pathophysiology of the disease and putative therapies. Besides lowering glycaemia, metformin down-regulates estrogen secretion, inflammation and oxidation. Metformin can be safely used before and during pregnancy, it is currently used in gestational diabetes. Metformin has shown to induce regression of endometrial implants in an endometriosis rat model. Study design, size, duration B6CBA/F1 female mice were randomly divided in groups and subjected to treatment: 1-Endometriosis(E) (n = 20); 2-Sham-operated(S) (n = 12); 3-Endometriosis with metformin(EM) (n = 20); 4-Sham-operated with metformin(SM) (n = 20). Endometriosis was surgically induced by heterologous transplantation of endometrium from one donor in receptors from the same strain mice. Implants were confirmed and monitored by ultrasound. 50mg/kg/day of metformin was orally administrated during 3 months to Groups 3 and 4. Half of mice in each group were mated to fertility study. Participants/materials, setting, methods Endometrial implants were monitored at 3 timepoints during the experiments. Fertility rates were assessed by the average number of fetuses in each group. Histological characterization of eutopic and ectopic endometrium was performed by H&E and Masson's trichrome staining. Immunofluorescence for PCNA and CYP17A1 proteins, markers of cell proliferation and estrogen secretion, respectively were performed. Western blotting quantification for these proteins is in course. Statistical analysis was carried out and significant differences were considered for p