INTRODUCTION
Obesity is considered one of the most significant health problems of our time due to its accompanying diseases such as diabetes, hypertension, and high cholesterol (1). It started in the 1980s and has continued worldwide regardless of the countries’ levels of development, being associated with various factors. Among these factors are environmental, genetic, endocrine factors, nutrition, and lifestyle (2). Despite the emphasis on nutrition, changes in nutrition and lifestyle have not been seen to completely solve the problem.
In the face of the rapidly increasing prevalence of obesity, the role of microorganisms in the formation of obesity has been considered (3). Based on this idea, the concept of ”infectobesity” has been put forward, and studies on this subject have shown that some microorganisms can cause obesity in animal models such as mice, chickens, and non-human primates. Since 1982, viruses associated with obesity have been identified, including Canine distemper virus (CDV), Rous-associated virus-7 (RAV-7), Borna disease virus (BDV), Scrapie agent prion, and SMAM-1 from animal viruses; and from human viruses, only Adenovirus 36 (Ad-36), Adenovirus 37 (Ad-37), and Adenovirus 5 (Ad-5) from the Adenoviridae family (4).
Adenoviruses are non-enveloped, icosahedral symmetric, and medium-sized viruses. All adenoviruses that infect humans share the same common genome; they contain a single linear and double-stranded DNA molecule. There are more than 50 serotypes infecting humans (5).
Adenoviruses associated with obesity are believed to cause triglyceride accumulation in fat cells (adipocytes) and differentiation of immature adipocytes (pre-adipocytes) into mature adipocytes (3). It has been determined that Ad-5 and Ad-37 increase the formation of fat cells in animals and contribute to the development of obesity. Ad-36 is the most studied human adenovirus to date, and its association with human obesity has been proven (6).
Leptin hormone is secreted by adipocytes of adipose tissue, reduces appetite, increases energy expenditure, stimulates the breakdown of fat cells, and inhibits lipid synthesis. It is known that insufficient synthesis of leptin leads to more fat storage. To investigate the mechanism of adipose tissue formation associated with adenovirus, the secretion of leptin in human pre-adipose cells infected with Adenoviruses was examined. It was found that in cells infected with Ad-37, leptin mRNA synthesis was suppressed, and lipid accumulation increased simultaneously. Additionally, changes in enzymes such as intracellular glycerol 3-phosphate dehydrogenase (GPDH) induced the transformation of pre-adipocytes into mature adipocytes (3).
The aim of our study is to investigate the seropositivity of Adenovirus 5 and 37 in blood samples taken from 48 obese patients and 42 normal weight individuals without underlying chronic diseases, not using any medication routinely, and without immune system problems, and whether there is a significant difference between obese and normal weight individuals. Increasing the number of studies on this subject and developing a new perspective on the infectious etiology of obesity will contribute to developing new treatment approaches for obesity and obesity-related diseases.