Nobumasa Kikuchi

Relationships between circulating leptin concentrations and other hormonal parameters in obese and non-obese women with polycystic ovary syndrome

AimTo clarify the role of leptin in women with polycystic ovary syndrome (PCOS), we analyzed whether serum leptin levels correlate with other hormonal parameters in obese and non-obese women with PCOS.MethodsWe studied 20 obese (body mass index, BM ≥25kg/ m2) and 20 non-obese (BMI < 25kg/m2) women with PCOS diagnosed by the existence of menstrual disturbance, elevated serum level of luteinizing hormone (LH) with normal follicle-stimulating hormone (FSH) and the characteristic polycystic appearance of the ovaries on transvaginal ultrasound images. Blood samples for LH, FSH, estradiol, testosterone (T), androstenedione (Δ4) and leptin were obtained, and the relationships between variables were examined by calculating Spearman correlation coefficients.ResultsMean levels of leptin, T and Δ4 in obese PCOS women were significantly higher than those in non-obese PCOS women, but this was not the case for BMI, bodyweight and waist to hip ratio. In all the 40 PCOS women considered together, there were significant positive correlations of leptin with BMI, waist to hip ratio, and Δ4 levels. However, in each group separately, serum leptin levels in obese PCOS women correlated only with BMI and bodyweight, whereas serum leptin levels in non-obese PCOS women correlated with serum Δ4 levels.ConclusionAlthough further study is needed to assess the role of leptin on ovarian function in non-obese women with PCOS, present findings do not support the fact that leptin is involved in the development of hormonal abnormalities in obese women with PCOS.

Ovarian follicular differentiation with prepubertal gonadotropin surges and gonadotropin priming in mice

Preantral follicles were mechanically isolated from the ovaries of 1.5 to 8 week old mice and cultured in vitro for 4 days in the presence or absence of either activin A or FSH. Plasma gonadotropin, estradiol and immunoreactive (IR) inhibin levels were measured. Cultured follicles showed stepwise changes in response to recombinant human (rh) FSH, with no response until 11 days, a gradual increase from 2 weeks, culminating in a strong response to rhFSH at 8 weeks. The response to activin A was vice versa. It enhanced the effect of rhFSH on preantral follicular growth of up to 4-week-old mice, but inhibited the effect of rhFSH in 8-week-old mice. The peak of the prepubertal gonadotropin surge was observed on day 11. Seven-day-old mice were treated with either luteinizing hormone releasing hormone (LHRH) or rhFSH or human chorionic gonadotropin (hCG) for 3 consecutive days from day 7, and follicles were collected on day 11. Those follicles showed enhanced response to rhFSH, no response to activin A, and an enhanced response to the combination of rhFSH and activin A, suggesting that the chronological changes in follicular response are a result of the prepubertal gonadotropin surge.