Akademik Veri Yönetim Sistemi
FABAD JOURNAL OF PHARMACEUTICAL SCIENCES, cilt.46, sa.2, ss.139-146, 2021 (Scopus)
Obesity is a chronic disorder with increasing prevalence worldwide
and occurs when energy intake is more 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, affect 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. Oxidative stress increment in adipose tissue
causes the development of metabolic syndrome in obese people. Also,
weight loss due to calorie restriction or exercise reduces oxidative
stress. Mitochondria is the essential source for ROS formation. In
the electron transfer system, reactive oxygen species forming due
to oxidative phosphorylation reactions are involved in various
physiological processes such as cell proliferation and differentiation.
Glutathione S-transferase M1 and T1 genes encode enzymes that
have oxidant-scavenging activities. Deletion polymorphisms in these
genes cause the absence of their corresponding enzymes. In this study,
we investigated the parameters associated with obesity such as body
mass index (BMI), TSH, glucose, satiety blood glucose, triglyceride,
and cholesterol levels, and deletion polymorphisms of GSTM1 and
GSTT1 genes in 152 patients diagnosed with obesity in a Turkish
population. No statistically significant relationship was found
between the parameters studied in obese patients and GSTM1 and
GSTT1 polymorphisms. More studies are needed to elucidate the
relationship of GSTM1 and GSTT1 polymorphisms with obesity