ESPE Abstracts

Background: Obesity has in males been associated with reduced testosterone levels during and after puberty. However, the onset and progress of puberty into fertility in obese boys remain inadequately evaluated.

Objective and hypotheses: We aimed to study testicular function at the end of pubertal development (15–24 years) in males with severe childhood-onset obesity (height-adjusted relative weight exceeding 160% before the age of 7 years).

Method: Fasting blood samples were analyzed for testosterone and several parameters characterizing pituitary function, adipose tissue, skeleton, and insulin resistance. Findings were compared with results in normal-weight age-matched control males. Results are expressed as median (range) and statistical analyses were performed with Mann–Whitney U-test and Kendall’s rank correlation test.

Results: BMI was 36.7 (26.3–62.1) kg/m² in obese subjects (n=20) in comparison to 22.1 (16.6–24.95) kg/m² in control subjects (n=17, P<0.001). Obese subjects had lower serum free testosterone levels than control subjects (pmol/l; 232 (111–505) vs 418 (118–720), P=0.002). Levels of serum LH, FSH, and estradiol did not differ between the groups. In the obese subjects, serum free testosterone level correlated positively with serum luteinizing hormone (τ=0.52, P=0.003), and negatively with BMI (τ=−0.42, P=0.009), serum leptin (τ=−0.51, P=0.002), and fasting plasma insulin (τ=−0.49, P=0.007). In the control group, testosterone level correlated positively with serum estradiol level (τ=0.42, P=0.02). Serum free testosterone did not correlate with age, serum FSH level, serum anti-Müllerian hormone level or serum hydroxyvitamin D level in either group.

Conclusion: Young men with childhood-onset obesity have lower testosterone levels than their normal-weight peers. The degree of testosterone reduction increased with increasing severity of obesity. Our findings indicate that severe childhood-onset obesity significantly impacts testicular function.