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.