Metformin prevents embryonic resorption induced by hyperandrogenisation with dehydroepiandrosterone in mice

• DOI: 10.1071/rd05099
• Publication Date: 2006-05-25T01:07:08Z
• Authors: M. E. Solano; E. Elia; C. G. Luchetti; V. Sander; G. Di Girolamo; C. Gonzalez; A. B. Motta
• Keywords: Blood Glucose; CD4-CD8 Ratio; Nitric Oxide; Mice; 03 medical and health sciences; 0302 clinical medicine; Pregnancy; https://purl.org/becyt/ford/3.1; Animals; Insulin; https://purl.org/becyt/ford/3; Progesterone; Mice, Inbred BALB C; Estradiol; Tumor Necrosis Factor-alpha; Ovary; Uterus; Dehydroepiandrosterone; Fetal Resorption; Metformin; 3. Good health; LYMPHOCYTE; Oxidative Stress; Female; MISCARRIAGE; Nitric Oxide Synthase; Hyperandrogenism; NITRIC OXIDE

The present study examined the mechanism by which metformin prevents dehydroepiandrosterone (DHEA)-induced embryonic resorption in mice. Treatment with DHEA (6 mg/100 g bodyweight, 24 and 48 h post implantation) induced 88 ± 1 % diminution of both serum oestradiol (E) progesterone (P) levels. However, when (50 mg/kg bodyweight) was given together DHEA, embryo (43 3% v. 35 5% controls) E P levels were not significantly different from controls. Glucose insulin increased DHEA-treated mice but administered these parameters similar to control values. ovarian oxidative stress diminished uterine nitric oxide synthase (NOS) activity; however, NOS activity Metformin treatment did modify percentage CD4+ CD8+ T cells axillar retroperitoneal lymph nodes prevented increase tumour necrosis factor α produced These results show that acts DHEA-induced modulating endocrine parameters, activity.