BACKGROUND: Hyperinsulinemia, which is related to obesity, played a pathogenic role in polycystic ovary syndrome (PCOS). However, the incidence of obesity in Japanese women with PCOS is different from that reported in patients with PCOS in Europe and USA. We should determine if insulin resistance occurs in Japanese PCOS. The purpose of this study is to assess the presence of insulin resistance in Japanese PCOS, while also considering obesity as a factor. METHODS: We divided the patients with polycystic ovary (PCO) into three groups based on body mass index and levels of gonadotropin. Nine obese PCOS, 34 normal body-weighted PCOS (luteinizing hormone (LH)/follicle stimulating hormone (FSH) >1.0) and 11 normal LH (LH/FSH </= 1.0), normal body-weighted PCO were studied. We compared those patients to 16 control subjects with normal ovulation or with hypothalamic anovulation. Eleven women in the control were normal body-weighted and five were obese. Patients were given an oral glucose tolerance test. Testosterone, plasma glucose and serum immunoreactive insulin after oral administration of 75 g dextrose were studied. We also compared glucose-intolerance [total plasma glucose (SigmaPG) and insulin (SigmaIRI), insulinogenic index (I.I.), fasting plasma glucose/immunoreactive insulin (FPG/IRI), homeostasis model assessment of insulin resistance (HOMA-R)] and testosterone among these groups. RESULTS: There were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between obese and normal body-weighted patients. Similarly, there were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls in the normal body-weighted group. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between the obese and the normal body-weighted PCOS. There were also significant differences in SigmaPG and I.I. between LH-dominant, normal body-weighted PCOS and normal LH PCO. CONCLUSION: Japanese PCOS might have insulin-resistance but the factor of obesity had a stronger effect on insulin-resistance than did the existence of PCOS. The possibility of a different type of glucose-intolerance was suggested in the patients with ultrasonographical PCO in whom gonadotropin secretion was abnormal.
BACKGROUND: Hyperinsulinemia, which is related to obesity, played a pathogenic role in polycystic ovary syndrome (PCOS). However, the incidence of obesity in Japanese women with PCOS is different from that reported in patients with PCOS in Europe and USA. We should determine if insulin resistance occurs in Japanese PCOS. The purpose of this study is to assess the presence of insulin resistance in Japanese PCOS, while also considering obesity as a factor. METHODS: We divided the patients with polycystic ovary (PCO) into three groups based on body mass index and levels of gonadotropin. Nine obese PCOS, 34 normal body-weighted PCOS (luteinizing hormone (LH)/follicle stimulating hormone (FSH) >1.0) and 11 normal LH (LH/FSH </= 1.0), normal body-weighted PCO were studied. We compared those patients to 16 control subjects with normal ovulation or with hypothalamic anovulation. Eleven women in the control were normal body-weighted and five were obese. Patients were given an oral glucose tolerance test. Testosterone, plasma glucose and serum immunoreactive insulin after oral administration of 75 g dextrose were studied. We also compared glucose-intolerance [total plasma glucose (SigmaPG) and insulin (SigmaIRI), insulinogenic index (I.I.), fasting plasma glucose/immunoreactive insulin (FPG/IRI), homeostasis model assessment of insulin resistance (HOMA-R)] and testosterone among these groups. RESULTS: There were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between obese and normal body-weighted patients. Similarly, there were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls in the normal body-weighted group. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between the obese and the normal body-weighted PCOS. There were also significant differences in SigmaPG and I.I. between LH-dominant, normal body-weighted PCOS and normal LH PCO. CONCLUSION: Japanese PCOS might have insulin-resistance but the factor of obesity had a stronger effect on insulin-resistance than did the existence of PCOS. The possibility of a different type of glucose-intolerance was suggested in the patients with ultrasonographical PCO in whom gonadotropin secretion was abnormal.