Congenital adrenal hyperplasia compromises both the development and the functioning of the adrenomedullary system.

A four-compartment (4C) model of body composition was used as a criterion to determine the accuracy of three-compartment (3C) and two-compartment (2C) models to estimate percent body fat (%BF) in prepubertal and pubertal boys (genital I & II, n = 17; genital III & IV, n = 7) and girls (breast I & II, n = 8; breast III & IV, n = 15). The 3C water-density (3C-H2O) and 3C mineral-density models, dual-energy X-ray absorptiometry, the Lohman age-adjusted equations, the Slaughter et al. skinfold equations, and the Houtkooper et al. and Boileau bioelectrical impedance equations were evaluated. Agreement with the 4C model increased with the number of compartments (i.e., body water, bone mineral) measured. Except for the 3C-H2O model, the limits of agreement were large and did not perform well for individuals. The mean %BF by dual-energy X-ray absorptiometry (23.6%) was greater than that of the criterion 4C method (21.7%). For the field methods, the Slaughter et al. skinfold equations performed better than did the Houtkooper et al. and Boileau bioimpedance equations. The hydration of the fat-free mass decreased (genital I & II = 75.7%, genital III & IV = 74.8%, breast I & II = 75.5%, breast III & IV = 74.4%) and the mineral content increased (genital I & II = 4.9%, genital III & IV = 5.0%, breast I & II = 5.1%, breast III & IV = 5.7%) with maturation. The density of the fat-free mass also increased (genital I & II = 1.084 g/ml, genital III & IV = 1.087 g/ml, breast I & II = 1.086 g/ml, breast III & IV = 1.091 g/ml) with maturation. All of the models reduced the %BF overprediction of the Siri 2C model, but only the 4C and 3C-H2O models should be used as criterion methods for body composition validation in children and adolescents.

Little is known about the influence of adiposity and hormone release on leptin levels in children and adolescents. We utilized criterion methods to examine the relationships among sex steroids, body composition (4 compartment), abdominal visceral and subcutaneous fat (magnetic resonance imagery), total subcutaneous fat (sum of 9 skinfolds), energy expenditure (doubly labeled water), aerobic fitness, and serum leptin levels in prepubertal and pubertal boys ( n = 16; n = 13) and girls ( n = 12; n = 15). The sum of skinfolds accounted for more variance in leptin levels of all girls [coefficient of determination ( R 2) = 0.70, P < 0.001] and all boys ( R 2 = 0.60, P < 0.001) than the total fat mass (girls, R 2 = 0.52, P < 0.001; boys, R 2 = 0.23, P < 0.001). Total energy expenditure, corrected for the influence of fat-free mass, correlated inversely with leptin ( R 2 = 0.18, P = 0.02). Gender differences in leptin disappeared when corrected for sex steroid levels or the combination of adiposity and energy expenditure. In multiple regression, the sum of skinfolds and free testosterone and estrogen levels accounted for 74% of the variance in leptin levels. We conclude that serum leptin levels are positively related to subcutaneous adiposity but negatively related to androgen levels. Energy expenditure may be negatively related to leptin levels by reduction of the adiposity, or a common genetic factor may influence both the activity and serum leptin levels.

The effects of intensity of run training on the pulsatile release of growth hormone (GH) were investigated in 21 eumenorrheic untrained women. The O2 consumption (VO2) at the lactate threshold (LT); fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM; peak VO2; maximal VO2; body composition; and pulsatile release of GH were measured. Subjects in both the at-lactate threshold (/LT, n = 9) and above-lactate threshold (greater than LT, n = 7) training groups increased VO2 at LT and FBLC of 2.0, 2.5, and 4.0 mM and VO2max after 1 yr of run training. However, the increase observed in the greater than LT group was greater than that in the /LT group (P less than 0.05). No change was observed for the control group (n = 5). No among- or within-group differences were observed for body weight, although trends for reductions in percent body fat (P less than 0.06) and fat weight (P less than 0.15) were observed in the greater than LT group, and both training groups significantly increased fat-free weight (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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We provide an in-depth review of the role of androgens in male maturation and development, from the fetal stage through adolescence into emerging adulthood, and discuss the treatment of disorders of androgen production throughout these time periods. Testosterone, the primary androgen produced by males, has both anabolic and androgenic effects. Androgen exposure induces virilization and anabolic body composition changes during fetal development, influences growth and virilization during infancy, and stimulates development of secondary sexual characteristics, growth acceleration, bone mass accrual, and alterations of body composition during puberty. Disorders of androgen production may be subdivided into hypo- or hypergonadotropic hypogonadism. Hypogonadotropic hypogonadism may be either congenital or acquired (resulting from cranial radiation, trauma, or less common causes). Hypergonadotropic hypogonadism occurs in males with Klinefelter syndrome and may occur in response to pelvic radiation, certain chemotherapeutic agents, and less common causes. These disorders all require testosterone replacement therapy during pubertal maturation and many require lifelong replacement. Androgen (or gonadotropin) therapy is clearly beneficial in those with persistent hypogonadism and self-limited delayed puberty and is now widely used in transgender male adolescents. With more widespread use and newer formulations approved for adults, data from long-term randomized placebo-controlled trials are needed to enable pediatricians to identify the optimal age of initiation, route of administration, and dosing frequency to address the unique needs of their patients.

We investigated whether gender affects the physiological relationships between the release of GH and age, body composition, and levels of physical fitness in humans. We studied 32 eumenorrheic females (age = 31 +/- 5 yr) and 12 males (age = 27 +/- 5 yr). Significant gender differences were found for peak oxygen consumption [VO2 peak = 40.5 +/- 6.9 (females) vs. 50.1 +/- 11.6 (males) ml/kg.min-1, P < 0.05] and body composition [hydrostatic weighing, percentage body fat = 28.7 +/- 5.4 (females) vs. 18.1 +/- 9.8 (males), P < 0.05] but not for body mass index [BMI = 23.7 +/- 3.1 (females) vs. 24.0 +/- 3.3 (males)]. Blood samples were drawn every 10 min for 24 h from 0800 h to determine integrated serum GH concentration [2350 +/- 1260 (females) vs. 3110 +/- 1760 (males) microgram/L x min]; females were studied during the early follicular phase (days 4-5) of the menstrual cycle. In females, a significant relationship existed between 24-h integrated serum GH concentration and age (r = -0.35, P = 0.05) but not BMI (r = -0.19, P = 0.29); the relationship between 24-h integrated serum GH concentration and VO2 peak (r = 0.31, P = 0.08) and percentage body fat (r = 0.29, P = 0.11) approached significance. In males, significant relationships existed between 24-h integrated serum GH concentration and age (r = -0.79, P = 0.002), percentage body fat (r = -0.75, P = 0.005), and VO2 peak (r = 0.58, P = 0.05) but not between 24-h integrated serum GH concentration and BMI (r = -0.53, P = 0.08). Standardized regression coefficients revealed that for each SD change in age, BMI, percentage body fat, or VO2 peak the associated change in 24-h integrated serum GH concentration was 1.9-2.6 times greater in males than in females. We conclude that age, percentage body fat (but not BMI), and fitness are related to 24-h GH release in young adults and that these relationships are considerably stronger in males than females.