Effect of High-Intensity Interval Training with Portulaca oleracea Supplementation on Liver LXα and PPARγ Receptors in Rats with Nonalcoholic Fatty Liver Disease

Introduction: Lifestyle modification through dietary interventions and exercise training is the main approach to treating nonalcoholic fatty liver (NAFLD). The aim of this study was to investigate the effect of high-intensity interval training (HIIT) with Portulaca oleracea supplementation on liver X receptor α (LXRα) and peroxisome proliferator-activated receptor γ (PPARγ) in the liver tissue of rats with NAFLD. Materials and Methods: In this experimental study, 30 male rats with a weight range of 160-185 g were divided into 2 main groups: NAFLD (n=25) and healthy control (n=5). Nonalcoholic fatty liver was induced in rats with 12 weeks of a high-fat diet. Five rats were sacrificed to confirm the establishment of NAFLD, and the remaining rats were divided into 4 subgroups: fatty liver control (n=5), P. oleracea supplement (n=5), HIIT (n=5), and HIIT+P. oleracea supplement (n=5). Rats in supplementation groups were given 400 mg/kg/day of dissolved P. oleracea powder. HITT consisted of 5 sessions a week of running with an intensity of 90% of maximum speed for 8 weeks. At the end of the study, LXRα and PPARγ ​​levels in liver were measured. Results: LXRα values were significantly lower in the HIIT+P. oleracea (P=0.002, effect size=0.63), HIIT (P=0.017, effect size=0.43), and P. oleracea groups (P=0.009, effect size=0.44) than in the fatty liver control group. LXRα values were significantly lower in the HIIT+P. oleracea group than in the HIIT (P=0.030) and P. oleracea groups (P=0.030). PPARγ values were significantly lower in the HIIT+P. oleracea (P=0.002, effect size=0.83), HIIT (P=0.030, effect size=0.60), and P. oleracea groups (P=0.004, effect size=0.71) than in the fatty liver control group. PPARγ values were significantly lower in the HIIT+P. oleracea group than in the HIIT group (P=0.030). Conclusion: HIIT with P. oleracea supplementation may be effective in the treatment of NAFLD disease by reducing LXRα and PPARγ and improving the regulation of fat production pathways in the liver.