Endocrine Abstracts

JOINT3491

Introduction: Leptin(L) is a signal from adipose tissue in the regulation of energy metabolism. Except of this other peripheral tissues contribute to its level and are being influenced through L receptors. Such have been found in the anterior lobe of the pituitary, gonads and in mammary epithelial cells. There is characteristic sexual dimorphism in L in both lean or obese individuals. Men have lower serum levels than women and this difference is found from puberty. L has a complex and bidirectional interplay with sex steroids. It has the ability to increase the activity of CYP19 aromatase thereby leading to increased estrogen (E) and in turn estrogens increase mRNA synthesis and L level. In addition, an inverse correlation with androgens has been reported and further in high-grade obesity high L has a suppressive effect on testosterone(T). On the basis of these data it could be speculated that L is part of the control of breast parenchymal proliferation and with other factors, could be involved in the development of pubertal gynecomastia (PG).

Aim: To investigate L in adolescents with PG at different stages of pubertal development with normal weight or obese and to compare it with L in a control group at the same age and BMI. To find a correlation between L and levels of sex steroids.

Methods: A total of 50 boys with PG, admitted to tertiary Pediatric endocrinology department in a single university hospital were included. They were divided into three groups according to pubertal stage: Tanner stage 2, mid pubertal stages 3-4 and a group with completed puberty. Anthropometric measurements, leptin and hormonal investigations were collected and compared with a group of 64 controls without PG matched in pubertal stage and anthropometrics.

Results: The investigation of leptin level in the three groups, matched for BMI and pubertal stage, did not prove statistically significant difference. Correlation was sought between L and sex hormones, free and biologically activeT, as well as the ratio of T and E2. Correlations were not found in all three groups of PG patients with normal weight or obese. А correlation was found in adolescents 3-4 Tanner stage in the control group with normal BMI: a strong positive between L and SHBG(r = 0,915, P <0,01) and correspondingly a strong negative correlation between L and freeT(r=-0,730, P <0,05), bioavailable T(r=-0,734, P <0,05), FAI(r=-0,914, P <0,01).

Conclusion: The presented study did not prove the role of L on development of PG, but confirmed its role on androgen levels in boys without PG.