山口 陽子

To examine the relationship between obesity and anovulation, 20 obese and anovulatory women (OA), 14 obese and regularly cycling women (OC), and 12 normal weight and regularly cycling women (NC) were endocrinologically studied. Parameters measured in serum were luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin (PRL) levels, and estrone (E1), estradiol (E₂), estriol (E₃), delta 4-androstene-dione (A), free testosterone (free T), and sex hormone binding globulin (SHBG). Blood samples were taken in the early follicular phase in OC and NC women.<BR>The body mass indices (BMI) of OA, OC, and NC women were 35.1± 0.9, 30.3±0.5, and 19.8±0.4 (mean±SEM), respectively. The mean BMI was significantly greater in OA and OC than in NC women (p<0.00001), and even in OA than in OC women (P<0.0002). Compared to NC women, OA women had increased concentrations of E₁ (84.0±6.1 vs 45.8±3.3 pg/ml, P<0.00001), A (2.77±0.25 vs 1.76±0.20 ng/ml, P<0.02), free T (2.59±0.30 vs 0.83±0.07 pg/ml, P<0.0002), LH (8.06±0.86 vs 4.99±1.23 mIU/ml, P<0.05), LH/FSH ratio (1.45±0.13 vs 0.78±0.20, P<0.05), and decreased concentration of SHBG (29.0±4.0 vs 90.9±9.8 n.mol/L, P<0.001). In contrast, there was no statistical difference in each parameter between OC and NC women, except for decreased SHBG levels (42.4±8.2 vs 90.9±9.8, P<0.001) in OC women. OA women also had increased levels of A (2.77±0.25 vs 1.82±0.21, P<0.02), free T (2.59±0.30 vs 1.20±0.28, P<0.005), LH (8.06±0.86 vs 4.03±0.71, P<0.005), and LH/FSH ratio (1.45±0.13 vs 0.94±0.17, P<0.05) compared to OC women, but there were no differences in FSH, PRL, E₁, E₂, and SHBG levels between the two groups. Serum E₃ levels were low (below 5pg/ml) in all women examined.<BR>In conclusion, the present study confirmed the previous findings that obese anovulatory women have PCO-like hyperandrogenic menstrual disorders. But, the results also showed that obese regularly cycling women did not have this endocine profile, suggesting that obesity itself may not be a primary causative factor of anovulation. Furthermore, the results imply that obesity itself, independent of androgens, may reduce serum SHBG level, and that the decrease in serum SHBG level may not always result in the increase in serum free T levels. However, we could not rule out the possibility that obesity may cause the sequence of endocrine events which result in anovulation as it proceeds, because the mean BMI value of OA women was significantly greater than that of OC women.