scholarly journals The effects of long-term metformin treatment on adrenal and ovarian steroidogenesis in women with polycystic ovary syndrome

2001 ◽  
Vol 144 (6) ◽  
pp. 619-628 ◽  
Author(s):  
J Vrbikova ◽  
M Hill ◽  
L Starka ◽  
D Cibula ◽  
B Bendlova ◽  
...  

OBJECTIVE: To evaluate adrenal and ovarian steroidogenesis before and after long-term treatment with metformin in women with polycystic ovary syndrome (PCOS). DESIGN AND METHODS: Twenty-four women with PCOS were evaluated before and after treatment (27+/-4 weeks) with metformin (1000 mg/day) using adrenocorticotrophin (ACTH), GnRH analogue and oral glucose tolerance (oGTT) tests. For statistical evaluation, ANOVA and Wilcoxon's test were used. RESULTS: In 58% of the women a significant improvement in menstrual cyclicity was observed. No significant change in basal steroid levels was found. After ACTH stimulation, a significant decrease in the activity of 3 beta-hydroxysteroid dehydrogenase in C(21) steroids (P<0.05) and in 17 beta-hydroxysteroid dehydrogenase (P<0.01) was observed, as was an increase in the activity of C17,20-lyase in the Delta(4) pathway (P<0.01). A significant growth in the dehydroepiandrosterone (DHEA)/DHEA-sulfate ratio (P<0.05) was detected. With regard to ovarian steroidogenesis, a significant decrease in the stimulated levels of testosterone (P<0.05), index of free testosterone (P<0.01), LH (P<0.05) and oestradiol (P<0.01), and an increase in the levels of 17-hydroxypregnenolone (P<0.05) were detected. In the indices of ovarian enzyme activities, we observed a significant decrease in 3 beta-hydroxysteroid dehydrogenase in C21 steroids (P<0.01), in C17,20-lyase in the Delta 5 pathway (P<0.01), in 17 beta-hydroxysteroid dehydrogenase (P<0.05) and in aromatase. In glucose metabolism, a tendency towards reduction in the homeostasis model assessment (HOMA)-R (for insulin resistance) and HOMA-F (for beta cell function) was detected. In addition, an increase in the levels of C peptide during oGTT was observed (P<0.01). CONCLUSIONS: Long-term metformin treatment reduced various steroid enzymatic activities both in the ovary and the adrenal glands, without apparent changes in basal steroid levels and in insulin sensitivity.

2006 ◽  
Vol 86 (1) ◽  
pp. 230-232 ◽  
Author(s):  
Paulina A. Essah ◽  
Teimuraz Apridonidze ◽  
Maria J. Iuorno ◽  
John E. Nestler

2008 ◽  
Vol 24 (7) ◽  
pp. 378-384 ◽  
Author(s):  
Joanna Jakubowska ◽  
Anna Bohdanowicz-Pawlak ◽  
Andrzej Milewicz ◽  
Jadwiga Szymczak ◽  
Grażyna Bednarek-Tupikowska ◽  
...  

2020 ◽  
Author(s):  
Liping Wang ◽  
Ke Hua ◽  
Wenwei Cai ◽  
Weiping Fu ◽  
Hongxia Zhang ◽  
...  

Abstract Background: Whether treatment with oral contraceptives (OC) and metformin can reduce anti-Müllerian hormone (AMH) levels in PCOS remains controversial. This study aims to investigate the effects of OC and metformin on serum AMH concentrations in women with polycystic ovary syndrome (PCOS). Methods: This prospective study included 120 women with PCOS. Patients were treated with OC (35 μg of ethinyl estradiol plus 2 mg of cyproterone acetate), metformin, or OC plus metformin for 3 months according to their different endocrine/metabolic disturbances. Forty-eight patients with hyperandrogenism (HA) were treated with OC, 32 patients with insulin resistance (IR) were treated with metformin, and 40 patients with HA and IR were treated with a combination of OC and metformin. Serum AMH levels were compared before and after treatment within each group.Results: AMH levels decreased significantly in both OC groups (from 12.54 ± 5.59 ng/mL before treatment to 9.03 ± 4.49 ng/mL after treatment, P < 0.01) as well as in the OC + metformin group (from 10.62 ± 4.57 ng/mL to 7.74 ± 3.19 ng/mL, P < 0.01). However, AMH concentrations remained unchanged in the metformin group, although insulin sensitivity was improved. Conclusion: Treatment with OC alone or OC plus metformin led to a significant reduction of serum AMH in PCOS patients with HA, while metformin treatment alone did not affect AMH levels in patients with IR.


2019 ◽  
Vol 104 (7) ◽  
pp. 2796-2800 ◽  
Author(s):  
Prapti Singh ◽  
Ariela Agress ◽  
Vanessa Kasarah Madrigal ◽  
Clara Magyar ◽  
Nora Ostrzega ◽  
...  

Abstract Context Ovarian hyperandrogenism from polycystic ovary syndrome (PCOS) and hyperinsulinemia from insulin resistance are modulators of ovarian follicle development. We report on a woman with PCOS and hyperandrogenism and severe insulin resistance from metabolic syndrome who received long-term GnRH analogue therapy preceding bilateral salpingo-oophorectomy for massive ovarian enlargement. Ovarian histological examination showed proliferating granulosa cells within antral follicles coexistent with serous cystadenofibromas, demonstrating a unique link between hyperinsulinemia and granulosa cell mitogenesis. Case Description A 30-year-old woman with PCOS with hyperandrogenism, severe insulin resistance from metabolic syndrome, and nonalcoholic steatohepatitis experienced abdominal pain from bilaterally enlarged ovaries. She had previously experienced a pulmonary embolism while taking oral contraceptives and hepatotoxicity from metformin and spironolactone therapies. Long-term GnRH analogue therapy to induce pituitary desensitization to GnRH successfully decreased gonadotropin-dependent steroidogenesis without improving insulin resistance. Despite GnRH analogue therapy, progressive ovarian enlargement in the presence of hyperinsulinemia from worsening metabolic function eventually required bilateral salpingo-oophorectomy for removal of massively enlarged ovaries. Histological examination showed both ovaries contained proliferating granulosa cells within antral follicles coexistent with serous cystadenofibromas. Conclusions In women with PCOS and hyperinsulinemia from severe insulin resistance due to metabolic syndrome, granulosa cell proliferation within antral follicles can occur despite long-term GnRH analogue therapy, implicating hyperinsulinemia as a granulosa cell mitogen in the absence of gonadotropin-dependent ovarian function.


2017 ◽  
Vol 108 (3) ◽  
pp. e245-e246
Author(s):  
M. Chen ◽  
P. Yang ◽  
H. Chen ◽  
S. Chen ◽  
H. Ho

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