Background: Previous infection with Adenovirus-36 (HAdv-D36) has been associated with adipogenesis and glycemic regulation in cell culture and animal models. In humans, HAdv-D36 antibodies correlate with increased obesity risk yet paradoxically enhance glycemic control across various demographics. This study assesses the association of HAdv-D36 seropositivity with obesity, lipid, and glycemic profiles among school-aged children. Methods: We evaluated 208 children aged 9-13, categorized by BMI z-scores into normal weight (-1 to +1), overweight (+1 to +2), and obese (>+3). Assessments included anthropometry, Tanner stage for pubertal development, and biochemical tests (relating to lipids, glucose, and insulin), alongside HAdv-D36 seropositivity checked via ELISA. Insulin resistance was gauged using Chilean pediatric criteria. Results: The cohort displayed a high prevalence of overweight/obesity. HAdv-D36 seropositivity was 5.4%, showing no correlation with nutritional status. Additionally, no link between HAdv-D36 seropositivity and lipid levels was observed. Notably, insulin levels and HOMA-RI were significantly lower in HAdv-D36 positive children (p < 0.001). No cases of insulin resistance were reported in the HAdv-D36 (+) group in our population. Conclusions: HAdv-D36 seropositivity appears to decrease insulin secretion and resistance, aligning with earlier findings. However, no association with obesity development was found in the child population of southern Chile.

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.

The aim of this study was to investigate the prevalence of Adenovirus-36 (Ad-36) in overweight and obese patients and the effects of this virus on some metabolic parameters.
The study included 236 female patients with body mass index (BMI) ≥ 25. The patients were separated into 2 groups as overweight (BMI: 25-29.99) and obese (BMI ≥ 30). To quantitatively determine the antibody (Ab) specific to adenovirus type 36 in the serum samples, the enzyme-immunoassay (EIA) method was used (AdV36-Ab, ELISA Kit, MyBioSource). Laboratoryparameters were compared between patients who are Ad-36 Ab positive and negative.
Of the total 236 patients, 82 (34.7%) were determined as Ad-36 positive and 154 (65.3%) were negative. Ad-36 Ab positivity was statistically significantly higher in the obese group (p = 0.018). The HOMA-IR index, triglyceride, total cholesterol, high-density lipoprotein, and low-density lipoprotein were found to be the same in both groups with no statistically significant differences(p > 0.05). Vitamin D levels were significantly higher in BMI ≥ 30 Ad-36 Ab positive group than negative group (p < 0.05).
The frequency ofAd-36 Ab positivity was significantly higher in the obese group than in the overweight group. These results can be considered to shed a different perspective from previous reports in literature as only overweight and obese females were included. To the best of our knowledge, this study is the first to have shown that Ad-36 has the effect of elevating the Vitamin D levels.

OBJECTIVE: The simple energy balance model of obesity is inconsistent with the available findings on obesity etiology, prevention, and treatment. Yet, the most commonly stated causes of pediatric obesity are predicated on this model. A more comprehensive biological model is needed upon which to base behavioral interventions aimed at obesity prevention. In this light, alternative etiologies are little investigated and thereby poorly understood.
RESULTS: Three candidate alternate etiologies are briefly presented: infectobesity, the gut microbiome, and circadian rhythms. Behavioral child obesity preventive investigators need to collaborate with biological colleagues to more intensively analyze the behavioral aspects of these etiologies and to generate innovative procedures for preventing a multi-etiological problem, e.g., group risk analysis, triaging for likely causes of obesity.

Obesity potentially arising from viral infection is known as \'infectobesity\'. The latest reports suggest that adenovirus-36 (Adv36) is related to obesity in adults and children. Our aim was not only to determine the Adv36 seropositivity in both obese and non-obese children and adults, but also to investigate correlations between antibody positivity and serum lipid profiles. Both Adv36 positivity and tumour-necrosis-factor-alpha, leptin and interleukin-6 levels were detected in blood samples collected from 146 children and 130 adults by ELISA. Fasting plasma triglycerides, total cholesterol and low-density lipoprotein levels were also measured. Adv36 positivity was determined to be 27·1% and 6% in obese and non-obese children and 17·5% and 4% in obese and non-obese adults, respectively. There was no difference with regard to total cholesterol, low-density lipoprotein, triglyceride, tumour-necrosis-factor-alpha and interleukin-6 levels (P > 0·05). However, there was a significant difference between groups in terms of leptin levels (P < 0·05). We determined the prevalence of Adv36 positivity in obese children and adults. Our results showed that Adv36 may be an obesity agent for both adults and children, parallel with current literature data. However, the available data on a possible relationship between Adv36 infection and obesity both in children and adults do not completely solve the problem.

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.

Chronic inflammatory diseases caused by obesity represent critical public health concerns worldwide. In these diseases such as metabolic syndrome, diabetes and atherosclerosis, adipose tissue acts as an endocrine organ that releases large quantities of inflammatory mediators into circulation. Besides classically recognized effectors on the development of obesity and resultant conditions, infection has attracted attention as an enhancer of chronic inflammatory diseases. Infectious diseases have long been associated with obesity, metabolic syndrome, diabetes and atherosclerosis. However, the infectious hypothesis for chronic inflammatory diseases has been challenged by inconclusive clinical trials. Nevertheless, the large body of evidence accumulated over decades on the association of infectious diseases with obesity, diabetes and cardiovascular disease should not be disregarded. Instead, re-formulation of hypotheses of the mechanisms by which microbes affect obesity-associated diseases may be required with an emphasis on the early events in the progression of such diseases and the multifactorial nature of pathogen-host interactions. This review focuses on pathogens that directly promote obesity and on pathogens that cause chronic infections and thereby enhance metabolic diseases in obese patients. A new perspective on the interaction between infections and obesity-related diseases may improve management of chronic inflammatory diseases that rank high among global threats to human health.