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