Akademik Veri Yönetim Sistemi
FABAD JOURNAL OF PHARMACEUTICAL SCIENCES, cilt.46, sa.3, ss.279-288, 2021 (Scopus)
Obesity is a chronic disorder with increasing prevalence worldwide
and occurs when energy intake is greater than energy expenditure.
Obesity is one of the factors that cause oxidative stress and arises from
an imbalance between the reactive oxygen species (ROS) and the cell’s
antioxidant defense system. Increasing ROS in obesity, influencing
the hypothalamic neurons, affects hunger and satiety control,
so correspondingly on body weight control. When ROS amount
increases, through DNA, protein and lipid oxidation, cell damage,
necrosis, and apoptosis take place. Tumor protein p53, the guardian
of the genome, is responsible for the regulation of genes involved in
apoptosis as well as energy generating metabolic pathways. In our
study, we investigated the TP53 (Arg72Pro) polymorphism in 151
patients diagnosed with obesity. TP53 mutation (rs1042522) was
determined by real-time PCR. In 8 patients, the TP53 mutation was
identified as carrying heterozygous (Arg72Pro) and in 143 patients
carrying homozygous (wild type) (Arg72Arg). No individual with a
homozygous mutant (Pro72Pro) genotype was found in the studied
group. Associations between TP53 genotypes and clinical obesity
parameters such as body mass index, thyroid stimulating hormon,
glucose, postprandial blood sugar, triglyceride and cholesterol levels
were compared statistically. According to the results of statistical
analysis, it was observed that TP53 polymorphism was associated
with insulin level. Genotype frequencies were also compared with
previous studies performed in control populations and found to be
different. This study shows that there may be a relationship between
TP53(Arg72Pro) polymorphism and obesity.