OBJECTIVE: Adenovirus-36 (Ad-36) seropositivity has been shown to be involved in the aetiology of obesity. The aim of this study was to examine Ad-36 positivity in obese and normal-weight patients with polycystic ovary syndrome (PCOS).
METHODS: There were two groups including 92 and 110 subjects. This study was a prospective case-control study. The enzyme-immunoassay method was used to quantitatively determine antibodies (Abs) specific to human Ad-36 in the serum samples. Age, body mass index (BMI), fasting glucose levels and insulin levels of the participants were recorded. The PCOS and control group patients were divided into two groups: the overweight group with BMI ≥25 kg/m2 and non-obese group with BMI <25 kg/m2.
RESULTS: Ad-36 Ab positivity in the PCOS group was found to be significantly higher than that in the control group (p < 0.001). Ad-36 Ab positivity was significantly higher in the PCOS obese group than in the control obese group (p < 0.001). Ad-36 Ab positivity and BMI ≥25 kg/m2 were identified as independent predictors of PCOS in logistic regression analysis.
CONCLUSIONS: Ad-36 Ab positivity was significantly higher in the obese/overweight PCOS patients. Obesity can be prevented in patients with PCOS by treating Ad-36.

Obesity which developes due to multifactorial reasons, was associated recently with human Adenovirus-36 (Ad-36). The aim of this study was to investigate the prevalence of Ad-36 antibodies in obese adults and also to investigate the DNA of Ad-36 in their adipose tissue. In this cross-sectional and case-control based study, 49 obese adults, with BMI ≥ 30 kg/m(2), and 49 non-obese adults, with BMI ≤ 25 kg/m(2), applied for esthetic purposes and were included in this study as patient and control groups, respectively. Adipose tissue samples, obtained by the lipoaspiration method, were studied by single-step PCR and nested-PCR methods. Simultaneously, the presence of Ad-36 antibodies and serum leptin and adiponectin levels were assessed by serum neutralization assay (SNA) and ELISA, respectively. Serum samples which didn\'t cause a cytopathic effect at ≥ 1:8 were accepted as positive. Ad-36 antibody was detected in 6 (12.2%) of 49 patients by SNA and was statistically significant (p < 0.05). Ad-36 DNA was not detected in any of the adipose tissue samples of the patient or control groups. Mean BMI and leptin levels were higher in the Ad-36-positive group, while adiponectin levels were found to be lower in the Ad-36-positive group. Although no statistically significant difference was found in cholesterol and triglyceride levels between the two groups (p > 0.05), lower mean serum cholesterol and triglyceride levels were found in the Ad-36-positive patients. In conclusion, we couldn\'t detect Ad-36 DNA in adipose tissue; however, we detected significantly higher Ad-36 antibody levels in the obese group compared to the non-obese group, according to the both univariant and multivariant analyses, suggesting that Ad-36 may play a role in obesity. There is a need for new and extended serial, particularly cohort and human-based, studies in order to have a clear understanding of the Ad-36-obesity relationship.