Delayed puberal development in obese males: possible role of hypogonadotropic hypogonadism

Background and aims: The objective of our work was to verify and quantify the presence of a puberal delay in a population of overweight and obese male subjects and to study the possible existence and role of hy-pogonadotropic hypogonadism. Materials and methods: 489 male subjects, normal weight (n = 240) and overweight/obese (n = 249), aged between 6-20 years, were observed. Patients with early and late puberty, hypogonadism, genetic diseases, genetic obesity, diabetes mellitus, pituitary and adrenal diseases were excluded from the study. Anthropomet-ric, laboratory and instrumental parameters were measured. They were then divided into Tanner stages, tes-ticular volume classes and age; for each stage, a comparison was then made between normal weight and overweight/obese for each parameter. Results: By relating the Tanner stages to testosterone levels, this was on average reduced by 107.74%(p<0.05) in overweight/obese subjects compared to normal weight controls [P1: 341.4 nmol/l vs 737.2 nmol/l; P2: 1327 vs 8158; P3: 2866.9 vs 10054; P4: 7715.5 vs 12411; P5: 10289 vs 15464]; the testicular volume was re-duced on average by 30.4%(p<0.05) [P1: 1.34 ml vs 0.96 ml; P2: 2.61 vs 5.58; P3: 3.97 vs 6.41; P4: 9.18 vs 9.82; P5: 10.1 vs 12.7]. Considering the subdivision into volumetric stages it was found as follows: age increased on average by 7.16%(p<0.05) [<4 ml: 11.4 age vs 10.2 age; 4-8 ml: 14.1 vs 13.6; 8-12 ml: 15.4 vs 14.9; >12 ml: 17.2 vs 15.5], testosterone reduced by 52.84%(p<0.01) [<4ml: 726.8 nmol/l vs 1363.7 nmol/l; 4-8 ml: 5990.5 vs 10043; 8-12ml: 9153.5 vs 14045; >12ml:11300 vs 16075], LH by 21.82%(p<0.05) [<4ml: 0.84 U/l vs 0.92 U/l; 4-8 ml: 2.43 vs 3.03; 8-12 ml: 3.18 vs 3.39; >12 ml: 2.67 vs 3.77], FSH by 14.43%(p<0.05) [<4ml:1.99 U/l vs 2.13 U/l; 4-8 ml: 3.16 vs 3.91; 8-12 ml: 3.69 vs 3.9; >12ml: 2.58 vs 3.13] and LH x testosterone by 86.78%(p<0.01) [<4ml: 1057.4 vs 3789.7; 4-8 ml: 18620 vs 34213; 8-12 ml: 30122 vs 48822; >12ml: 30323 vs 62828]. Using age classes: testicular volume was reduced by 7.47%(p<0.01) [<8 yr: 0.86 ml vs 0.54 ml; 9-11 yr: 2.06 vs 0.91; 12-15 yr: 6.47 vs 7.49; 15-20 yr: 11.08 vs 13.07], testosterone by 60.6%(p<0.01) [<8yr: 215.2 nmol/l vs 178.2 nmol/l; 9-11 yr:1108 vs 673.9; 12-15 yr: 5519.2 vs 10319; 15-20 yr: 10048 vs 15956], LH by 12.52%(p<0.05) [<8 yr: 0.21 U/l vs 0.29 U/l; 9-11 yr: 0.73 vs 0.51; 12-15 yr: 2.13 vs 2.77; 15-20 yr: 3.88 vs 4.25] and FSH by 13.19(p<0.05) [<8 y: 0.71 U/l vs 1.34 U/l; 9-11 yr: 1.82 vs 1.70; 12-15 yr: 3.01 vs 3.58; 15-20 yr: 3.80 vs 3.95]. Conclusion: Overweight and obese male subjects showed a testicular volume reduced (-30%) and testos-terone halved compared to normal weight subjects with consequent delay in pubertal development. They had a reduction in the secretion of FSH and LH which should on the contrary be increased. The reduction of testic-ular volume, testosterone and gonadotropins probably negatively influence spermatogenesis and could be a cause of reduced male fertility.