• Clinical and Experimental Reproductive Medicine
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• v.33 no.4
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• pp.245-251
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• 2006

Objective: We analyzed quantification of mitochondria DNA (mtDNA) to investigate the relationship of mitochondria and pathogenesis of PCOS. Materials and Methods: Peripheral blood samples were collected from 28 patients with PCOS who were under the inclusion criteria for PCOS and from 28 healthy controls. Genomic DNA was used to analyze real-time PCR for mtDNA copy number quantification. The mtDNA copy number was compared between the control and PCOS groups. All data was expressed as mean ${\pm}$ SD. Statistical analysis was assessed by t-test. Results: In this study, the mtDNA $C_T$ was $11.67{\pm}0.422$ in PCOS patients and $11.51{\pm}0.722$ in control group, respectively. The mtDNA copy number was $1726410.71{\pm}407858.591$ the patients of in PCOS and $2167887.51{\pm}252459.28$ in control group (p=0.08), respectively. Conclusion: In our study, using real-time PCR, there was a tendency of lower mtDNA copy number in the patients of PCOS when comparing to the control group even though statistical difference was not significant. However, more extensive analysis is required to clarity relationship between mtDNA copy number and pathogenesis of PCOS.

• Clinical and Experimental Reproductive Medicine
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• v.29 no.1
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• pp.67-76
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• 2002

Objective: To assess the difference of baseline hormonal status and pathophysio logy, and confirm the risk factors for long term complication according to Body Mass Index in women with polycystic ovary syndrome. Materials and Methods: Serum level of LH, FSH, Estradiol, Prolactin, Testosterone, DHEA-S, fasting insulin were measured and 100 gm oral glucose tolerance test and endometrial biopsy were performed in total 75 chronic anovulation patients and 20 normal cycling infertility patients. 95 evaluated patients were divided into 3 groups including patients with chronic anovulation having BMI below 25, BMI beyond 25.1, normal cycling infertility patients, Group 1 (n=39), Group 2 (n=36), Group 3 (n=20), respectively. Statistical analysis was performed respect to relationship between BMI and measured hormone level, sum of glucose level during 100 gm OGTT, insulin resistance using t-test, ANOVA test, Post Hoc test, Mann-Whitney test. p<0.05 was considered as statistically significant. Results: Serum LH level and LH/FSH ratio was significantly higher in Group 1, compared than Group 2 or 3 (p<0.05), BMI and LH, LH/FSH ratio was negatively correlated (r=-0.351, r=-0.318). There was no significant difference according to BMI in FSH, testosterone, estradiol, prolactin, DHEA-S level. Fasting insulin and sum of glucose level during 100 gm OGTT were significantly higher in Group 2 compared than Group 1 or Group 3 (p<0.05), there was no significant difference between Group 1 and Group 3. Insulin resistance was more frequently identified in Group 2 compared than Group 1 (p=0.001). Conclusions: BMI and LH, LH/FSH ratio were negatively correlated, so clinical significance of LH, LH/FSH ratio in diagnosis of PCOS may be attenuated by increasing body weight. Overweight patients with chronic anovulation may be the risk group for developing insulin resistance, hyperinsulinemia, glucose intolerance, later type 2 DM. Hyperinsulinemia may operate mainly in overweight chronic anovulation patients in development of hyperandrogenism.