ESPE Abstracts (2014) 82 P-D-3-1-924


aFlorence Nightingale Hospital, Istanbul, Turkey; bKatip Çelebi Univeristy, Izmir, Turkey; cDokuz Eylul University, Izmir, Turkey

Background: It has been reported that there is a relationship between circulating leptin and sex steroid hormones and leptin is able to stimulate estrogen secretion by increasing aromatase activity in adipose stromal cells and breast tissue. Leptin receptors have been also shown in mammary epitheleal cells and it has been suggested that leptin is involved in the control of the proliferation of both normal and malignant breast cells.

Objective and hypotheses: To investigate circulating leptin levels in boys with pubertal gynecomastia.

Method: 20 boys with pubertal gynecomastia who were in early puberty and had no obesity and 20 healthy individuals matched for age, pubertal stage, and BMI with the study group were enrolled in the study. Body weight, height and left mid arm circumference (MAC) and left arm triceps skinfold thickness (TSF) were measured and BMI was calculated. A fasting blood sample was collected and routine hormonal parameters including prolactin, beta human corionic gonadotrophin, total and free testosterone, estrodiol, LH, FSH, and restenodione (AS) and DHEAS levels were studied. Serum leptin levels were analyzed.

Results: The mean ages of the study and control group were not different (13.9±0.89 and 14.2±0.66 respectively). No significant difference were detected for BMI, MAC, TSF, and hormonal levels except leptin. Leptin levels were found significantly higher in the study group compared with the healthy controls (5.58±0.82 and 2.39±0.29, P<0.001). No correlation could be determined between serum leptin levels and hormonal parameters.

Conclusion: The presence of higher leptin levels in boys with pubertal gynecomastia indicates that leptin maybe involved in the pathogenesis of pubertal gynecomastia. The role of circulating leptin in pubertal gynecomastia is probably related to increase in estrogen and/or estrogen/and rogen ratio by stimulating effect of leptin on aromatase enzyme activity in both adipose and breast tissues, or a direct stimulating effect of leptin On mammary epitheleal cells or increase in sensitivity of breast epitelyumeal cells to estrogen with inducing functional activation of estrogen receptors by leptin in breast tissue.

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