Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

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

Kocazeybek B., Saribas S., Ergin S.

Laboratory Study with a reported sample of 33 on Chronic Inflammation, published in Med Hypotheses (2015) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Med Hypotheses (2015)
Country
United States
Reported sample size
33
Source database
PubMed
PMID
26394544
DOI
10.1016/j.mehy.2015.08.020

Abstract (original English)

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. A

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AdenoviridaeAdiponectinAdipose TissueAdultCase-Control StudiesDNA, ViralEnzyme-Linked Immunosorbent AssayGynecomastiaHumansInflammation

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research