The effects of leptin on redox status and asprosin and acylation stimulating protein in the liver of obese rats

Aim: The aim of our study is to investigate the effects of leptin on asprosin, acylation stimulating protein and redox status in the liver of obese rats and to evaluate its role and therapeutic potential in the pathophysiology of obesity. Materials and Methods: 32 Wistar Albino rats were randomly divided into groups as control, control+leptin, obesity, obesity+leptin. To create an obesity model, high fat diet for rats was presented ad libitum for 12 weeks, and at the end of this period, phosphate buffer solution (2mL/kg) was administered to the control and obese groups, leptin (0.1mg/kg) was administered to the obese+leptin and control+leptin groups for five days. After this period, the rats were sacrificed and their liver tissues were taken and the parameters were analyzed with ELISA kits, colorimetric kits, spectrophotometric and spectrofluorometric methods. Results: Concentrations of asprosin, acylation-stimulating protein, inflammation and biomarkers indicating increased oxidative stress were found to be significantly higher in obese groups compared to control groups. The specific activities of ALT, AST, LDH enzymes, which are considered biomarkers of liver tissue damage, are significantly higher in the obese group compared to controls, and there is a significant decrease in all three biomarkers as a result of exogenous leptin application. No statistically significant relationship was found between other groups. Conclusion: Increased systemic inflammation and disruptions in redox homeostasis and increased tissue damage biomarkers in liver tissue in obese groups suggest obesity-related liver complications. Decreased ALT, AST, LDH activities in obese groups as a result of leptin injection may indicate the therapeutic potential of leptin on liver tissue. We believe that our study may contribute to elucidating the pathophysiology of obesity.