Author(s): CHEN, J., WANG, C., YANG, W., YE, B., NING, Z., Institution: JIANGSU RESEARCH INSTITUTE OF SPORTS SCIENCE, Country: CHINA, Abstract-ID: 467

INTRODUCTION:
Mitochondrial dysfunction in hepatocytes is closely associated with metabolic dysfunction-associated fatty liver disease (MAFLD). Although aerobic exercise is known to benefit MAFLD, the underlying mechanisms remain to be fully elucidated. This study examines how aerobic exercise modulates mitochondrial function to alleviate MAFLD progression.
METHODS:
Rats with high-fat diet (HFD)-induced MAFLD were subjected to 8 weeks of aerobic treadmill training. A subgroup of exercised rats received the AMPK inhibitor Compound C. Assessments included metabolic profiling, liver histology, mitochondrial dynamics markers, and AMPK-PPARα-FGF21 pathway activity.
RESULTS:
HFD induced obesity, insulin resistance, hepatic steatosis, and mitochondrial fission/fusion imbalance. Exercise reversed these alterations and activated AMPK-PPARα-FGF21 signaling. AMPK inhibition abolished exercise benefits, reinstating steatosis and mitochondrial dysfunction while suppressing PPARα-FGF21 activation.
CONCLUSION:
Aerobic exercise ameliorates MAFLD by restoring mitochondrial homeostasis through activation of the AMPK-PPARα-FGF21 pathway, highlighting AMPK as a pivotal therapeutic target for MAFLD intervention.