Effect of rosiglitazone on endocrine, metabolism and ovulatory performance in patients with polycystic ovary syndrome and insulin resistance

Abstract

The effect of rosiglitazone on endocrine, metabolism and ovulatory performance in the paitents with polycystic ovary syndrome (PCOS) and insulin resistance was investigated. Twentyfive patients diagnosed as having polycystic ovary syndrome (PCOS) combined with insulin resistance were treated with rosiglitazone for 12 weeks. Before and after treatment, serum luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E2), testosterone (T), androstenedione (A), sex hormone binding globulin (SHBG), insulin and glucose concentration, total cholesterol, triglycerides (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholestero (LDL-C), apolipoprotein A, apolipoprotein B levels and ovulatory performance were determined. The results showed that after treatment serum insulin levels was decreased significantly (P<0.01). The HDL-C was increased while LDL-C decreased significantly (P<0.05,P<0.01). The serum LH, T, A concentrations and the ratio of LH/FSH were decreased, while SH-BG levels increased significantly (P<0.01). The ovulation rate during clomiphene citrate therapy was 72%, significantly higher than that before treatment. It is likely that reduction of hyperinsulinemia that is produce by rosiglitazone may effectively improve the endocrine, metabolism and ovulatory performance in the patients with PCOS and insulin resistance.

Keywords

polycystic ovary syndrome / rosiglitazone / insulin resistance / ovulation

References

[1] FranksS. Polycystic ovary syndrome. N Engl J Med, 1995, 333: 853-853

[2] MeirowD, YossepowitchO, RosierA, et al.. Insulin resistant and non-resistant polycystic ovary syndrome represent two clinical and endocrinological subgroups. Hum Reprod, 1995, 10: 1951-1951

[3] PoretskyI, PiperB. Insulin resistance. Hypersecretion of LH and a dual-detect hypothesis for the pathogenesis of polycystic ovary syndrome. Obstet Gynecol, 1994, 84: 613-613

[4] ChangB C, ZhengS X. Insulin enhanced sensitized agent-Application of rosiglitazone in diabetes mellitus. Guo Wai Yi Xue Nei Fen Mi Xue Fen Ce (Chinese), 2001, 21(1): 34-34

[5] DunaifA. Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesia. Endocr Rev, 1997, 18(10): 774-774

[6] NestlerJ E, DanielaJ, JakubowiezM D. Decrease in ovarian cytochrome p450sc17α activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome. N Engl J Med, 1996, 335: 617-617

[7] LeroithD, WernerH, RobertsC T, et al.. Molecular and cellular aspects of the insulin like growth factor-1 receptor. Endocr Rev, 1995, 16: 143-143

[8] NomuraM, KinoshitaS. (3-substituted benzyl) thiazolidine-2, 4-diones as structurally new antihyperglycemic agents. Bioorg Med Chem Lett, 1999, 9: 533-533

[9] HasegawaI, MurakawaH, SuzukiM, et al.. Effect of troglitazone on endocrine and ovulatory performance in women with insulin resistance-related polycystic ovary syndrome. Fertil Steril, 1999, 71: 323-323

[10] RobinsonS, HendersonA D, GeldingS V, et al.. Dyslipidemia is associated with insulin resistance in women with polycystic ovaries. Clin Endocrinol, 1996, 44: 277-277

[11] MeirowD, RazI, YossepowitchO, et al.. Dyslipidemia in polycystic ovarian syndrome: different groups, different aetiologies?. Hum Reprod, 1996, 11: 1848-1848

[12] DunaifA. Hyperandrogenic anovulation (PCOS): a unique disorder of insulin action associated with an increased risk of NIDDM. Am J Med, 1995, 98: 33-33