ESPE Abstracts

Background: Kisspeptins, ligands of G protein-coupled receptor 54 (GPR54) encoded by the KiSS-1 gene, have recently emerged as key players of the gonadotropic axis. It was found that KiSS-1/GPR54 system plays an important role in the neuroendocrine control of gonadotropin secretion, brain sex differentiation, puberty onset and fertility. It is important to know if the kisspeptin serum level could be used as a diagnostic criterion to the stage of puberty or impairment of it in boys.

Objective: To investigate the possible relation between the serum level of kisspeptin and different stages of puberty in healthy boys and boys with delay of puberty onset due to hypogonadotropic hypogonadism.

Methods: 39 boys in total were examined. They were divided into three groups. Group 1 (control, prepubertal boys aged 4–10 years old, Tanner I, n=15). Group 2 (control, pubertal boys aged 14–17 years old, Tanner IV-V, n=16). Group 3 (hypogonadotropic boys aged 14-17 years old, Tanner I, n=8). Hypogonadotropic hypogonadism in boys was confirmed by the median (Me) of basal level of testosterone (T) 0.33 nmol/l, Me LH 0.3 mU/l, a Gn-RH-stimulated LH value less than 5 IU/l. In all the groups the serum level of kisspeptin was examined by immunoassay (Cloud-Clone Corp., USA). The data was expressed as mean values (M+m).

Results: The level of kisspeptin in blood in group 1 and 2 did not have any differences (16.27+2.23 pg/ml and 14.11+1.71 pg/ml respectively, P>0,05). Unlike the above, the level of kisspeptin in group 3 was significantly higher than in both groups 1 and 2 (50.91+14.43 pg/ml as opposed to 16.27+2.23 pg/ml, P<0.01; 50.91+14.43 pg/ml as opposed to 14.11+1.71 pg/ml, P<0.002 respectively).

Conclusions: The serum level of kisspeptins was found to be equal in boys, sexually developed regardless of their age and stage of puberty. In contrast, the level of kisspeptins was significantly higher in boys affected with gonadotropic hypogonadism. It can be caused by GPR54 insensitivity or loss of biological activity of kisspeptin. The latter condition can be corrected by novel therapeutic technologies such as treatment with exogenous kisspeptin.