Reproductive Hormones

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Puberty may begin early in tall overweight children with advanced skeletal age (320). Pubertal elevations of follicular-stimulating hormone have been observed in the 7- to 9-year-old girls, without any changes in luteinizing hormone levels (320). This is compounded by an adiposity-related decrease in circulating concentrations of sex hormone-binding globulin (SHBG). This results in a higher fraction of free or unbound serum sex steroids that are more bioactive than the ones in lean subjects. In general, the SHBG abnormalities correlate with the degree of obesity, which are reversed with weight loss. Low serum estradiol levels and elevated progesterone levels have been observed in young prepubertal and early pubertal obese girls compared with age-matched lean girls (320).

As discussed above hyperinsulinemia is usually accompanied by hyperandrogenism, which leads to hirsutism and PCO (48). Amenorrhea, oligomenorrhea, and/or dysfunctional uterine bleeding are common among obese adolescent females. Some of these patients will also develop PCO syndrome (48-50). PCO is now recognized as a component of the IRS (Vol. 1; Chaps. 11 and 13). Insulin-lowering agents have become the norm in the management of PCO (51).

Obese adolescent boys appear to have an attenuated testicular response to human chorionic gonadotropin, This is probably an artifact of decreased SHBG. Indeed, Glass (65) demonstrated that despite a decrease in SHBG levels, free testosterone levels and dihydrotestosterone levels remain normal in obese subjects. Aromatization of androgens to estrogens by adipose tissue, in males, appears to be enhanced without clinical feminization (65). However, free and total testosterone levels may be diminished in morbidly obese males. This is commonly associated with decreased gonadotropin levels, suggesting some degree of hypogonadotropic hypogonadism (248). These alterations in pituitary and gonadal hormones return to normal range with weight loss (341). Indeed, since circulating leptin correlates directly with fat mass and serves as a permissive signal for stimulation of reproductive system, its rising serum concentrations in obesity may alter reproductive function in obese individuals (342).

Conversely, precocious puberty may lead to obesity. Children with idiopathic precocious puberty prior to treatment show no differences in regard to lean or fat mass. However, during long-term treatment with gonadotropin-releasing hormone (GnRH) children present a reduction of lean mass and increased fat mass which may lead to obesity (343). This may be due to a shortening of the prepubertal growing period and by the so-called menopausal effect of the treatment. In another study, both boys and girls with precocious puberty had BMI scores above the 85th percentile prior to and during treatment with GnRH. After treatment the scores still remained above the 85th percentile suggesting that children with precocious puberty are prone to obesity though treatment of precocious puberty itself did contribute to obesity (344).

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