Obesity and serum luteinizing hormone level have an independent and opposite effect on the serum inhibin B level in patients with polycystic ovary syndrome

Objective: To elucidate whether the negative effect of obesity on the serum inhibin B level that we previously reported is specific or not to polycystic ovary syndrome (PCOS) and whether it may explain the wide interindividual variability in serum inhibin B levels found in patients with PCOS. Design: Prospective study. Setting: Reproductive endocrinology unit of an academic medical center. Patient(s): One hundred thirty-four consecutive patients with PCOS (mean age, 27.4 ± 4.7 years; mean body mass index [BMI], 28.3 ± 7.6 kg/m 2; BMI > 25, 53%) and in 78 control women (mean age, 30.1 ± 4.1 years; mean BMI, 24.3 ± 4.9; BMI > 25, 34%). Intervention: Blood sampling was performed in the early follicular phase in patients and in control women. Main Outcome Measure(s): BMI and waist circumference (WC), serum levels of inhibin B, LH, FSH, E 2, androstenedione, T, fasting insulin, and leptin were assessed in all subjects. Result(s): No difference was observed in the mean inhibin B level between patients and controls. The BMI and WC correlated negatively with inhibin B in patients with PCOS and in controls, with similar regression slopes, thus indicating that the influence of obesity on inhibin B is not specific to PCOS. In addition, we found a positive relationship between serum LH and inhibin B levels in PCOS. There was no significant interaction between the effects of BMI and LH on the serum inhibin B levels by analysis of variance (ANOVA). The mean serum inhibin B level in patients with PCOS with high serum LH (i.e., >the 90th percentile of LH in controls) was significantly higher than in those patients with normal LH or in controls. The highest mean inhibin B level was noted in nonobese patients with PCOS with high LH levels (121.0 ± 51.2 pg/mL), while nonobese patients with PCOS with normal LH levels and obese patients with normal LH or high LH levels had similar mean levels (94.5 ± 40.0, 84.9 ± 34 and 91.6 ± 51.7 pg/mL, respectively). Conclusion(s): We confirm that obesity has a negative effect on inhibin B serum level, which is not specific to PCOS. Obesity and excess LH, acting oppositely and independently on inhibin B production, may explain the discrepancies between the previous reports studying serum inhibin B level in patients with PCOS. Further work is required to elucidate the mechanisms underlying the antagonistic effects of LH and obesity on inhibin B production in patients with PCOS.