Gynecomastia is highly prevalent worldwide and Adenovirus-36 (Ad-36), recently implicated in increased adipose tissue deposition due to its affinity for adipose tissue, is a potential etiological agent in the development of
obesity and therefore we hypothesized that Ad-36 may also play a role in the development of
gynecomastia by possibly accompanying increased regional adiposity. To support our hypothesis, we conducted a study that included 33 adult males with
gynecomastia (PG) and 15 adult males as the patient control group (HCG).
Leptin and
adiponectin levels were monitored using ELISA. A significant difference in Ad-36 antibody positivity was found between the groups (p<0.05). Average
leptin levels were found to be higher, but average
adiponectin levels were found to be lower in Ad-36 Ab(+) patient group. No Ad-36
DNA was detected in any tissue samples. 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.