The role of Ad-36 as a risk factor in males with gynecomastia

In conclusion, we hypothesize that low-grade chronic inflammation, which was caused by Ad-36 infection, possibly caused an increase in circulating leptin. This in turn may have caused an increase in local or circulating estrogens and/or the estrogen/androgen ratio by stimulating the aromatase enzyme activity in adipose stromal cells and breast tissues. We suggest that gynecomastia may develop following an increase in aromatase enzyme activity, by which more oestrogen is produced and the estrogen-androgen balance disrupted. Also, regional adipose tissue enlargements may cause the excessive production of estrogens leading to gynecomastia. Adipose tissue has been recognized as a major endocrine organ in recent years. Another plausible explanation is excessive aromatization of androgens to estrogens by peripheral adipose tissue may promote gynecomastia in males. Moreover, our results suggest that there might be a relationship between Ad-36 and gynecomastia.