Expression levels investigation of autophagy related genes in diet induced experimental obesity model

Obesity, which is a metabolic disease, which has become one of the most important health problems of especially developed societies throughout the world in recent years, and which has become a bigger problem than malnutrition and infectious diseases, which have been the biggest problems until now, unhealthy diet, lifestyle away from sports, stress When work and general lifestyle are added, it also causes related diseases such as type 2 diabetes mellitus, hypertension, coronary heart diseases, certain types of cancer, sleep breathing disorder and osteoarthritis. Obesity is defined by the Body Mass Index (BMI). Genetic susceptibility, easy access to high-energy foods, and decreased physical activity can be listed as the main causes of obesity becoming a global epidemic, especially in modern societies. Obesity should now be described as an epidemic that threatens global health, rather than an individual cosmetic or visual nuisance. Autophagy is responsible for levels of long-lived proteins and damaged or functionally unnecessary intracellular structures. It is the process necessary for the maintenance of cellular homeostasis, activated by starvation (to provide ATP-producing substrates, eg amino acids) and other stress-inducing conditions. Any irregularity in the mechanism plays a role in many disorders and aging. It is known that hepatic autophagy is impaired in obesity and diabetes, and its regulation increases insulin sensitivity. Autophagy is an intracellular degradation system that delivers cytoplasmic components to the lysosome. Despite its simplicity, recent advances have shown that autophagy plays a wide variety of physiological and pathophysiological roles that are sometimes complex. For these reasons, ATG3, ATG5 and ATG8 genes, whose relationship with autophagy has been proven by literature and studies, will be studied in experimental animal model samples. In our study, RNA isolation, cDNA synthesis, real-time PCR (RT-qPcR) methods were used. According to the comparative statistical analysis made between the liver and adipose tissues of the C57BL6J animal model in the two experimental groups and the control group (20 animals each), the experimental groups and the control group adipose and liver tissue data, ATG5 in the experimental group 1 (D1) adipose tissue samples (Fold change -1.13: p value -0.001: 95% confidence interval -0.75-1.83) and ATG8 (Fold change -0.23: p value -0.019: 95% confidence interval -0.21-2.46) The expression levels were increased and found to be significant. An increase in the expression level of ATG8 (Cold Change -0.60: p value -0.001: 95% confidence interval -1.47-3.73) was observed in D1 group liver tissue samples. In the liver tissue samples of the control group, ATG3 (Cold Change-2.81: p value-0.031: 95% confidence interval-0.19-3.83) and ATG5 (Cold Change-2.39: p value-0.016: 95% confidence interval-0, 36-3.25) expression levels were increased and found to be significant. The results of the analysis based on the data of the experimental group 2 (D2) and control group adipose tissue samples showed that ATG5 (Colle Change-1.65: p value-0.007: 95% confidence interval-0.23-1.35) and ATG8 (Fold Change-1.35) in the D2 group. -0.19: p value-0.008: 95% confidence interval -0.45-2.68) was found to be significant and increased in expression levels. As a result of the analysis performed according to the liver tissue samples of the experimental group 2 (D2) and control group, ATG8 (Cold Change-0.61: p value-0.001: 95% confidence interval-0.24-3.42) in liver tissue samples and ATG5 ( Fold Change-2.01: p value-0.015: 95% confidence interval-0.33-2.88) expression levels were found to be increased and significant. ATG3, ATG5 and ATG8 autophagy gene regions, which are the subject of our study, and studies conducted according to international literature show that this research should continue, and we think that increasing the number of samples related to this subject and the obtained data will connect the relationship between obesity, a metabolic disease, and cancer to a more solid basis. We think that genes are potential candidate genes in diagnosis.