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Luteolin Relieves Metabolic Dysfunction-Associated Fatty Liver Disease Caused by a High-Fat Diet in Rats Through
Pongsakorn Taweesap1, Prapassorn Potue1, Juthamas Khamseekaew1
1Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
International Journal of Molecular Sciences
|May 7, 2025
Summary
Luteolin, a natural compound, effectively treats metabolic dysfunction-associated fatty liver disease (MAFLD) in rats by improving metabolic health and reducing inflammation. It also enhances key protein expressions linked to metabolic regulation.
Area of Science:
- Biochemistry
- Pharmacology
- Hepatology
Background:
- Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing global health concern.
- Luteolin exhibits known antioxidant and anti-inflammatory properties.
- Understanding natural compounds' therapeutic potential for MAFLD is crucial.
Purpose of the Study:
- To investigate the efficacy of luteolin in ameliorating high-fat diet (HFD)-induced MAFLD in a rat model.
- To explore the underlying molecular mechanisms of luteolin's action on MAFLD.
Main Methods:
- MAFLD was induced in rats using a high-fat diet supplemented with fructose.
- Luteolin (50 or 100 mg/kg/day) or metformin was administered to MAFLD rats for 4 weeks.
- Metabolic parameters, liver injury, oxidative stress markers, and protein expressions (AdipoR1, AMPK, PPAR-γ) were assessed.
Main Results:
- Luteolin significantly improved metabolic parameters, including reduced body weight, blood glucose, insulin, lipids, and blood pressure.
- Luteolin attenuated hepatic injury, inflammation, and oxidative stress (reduced malondialdehyde, increased catalase).
- Luteolin treatment led to increased plasma adiponectin and upregulated hepatic AdipoR1, AMPK, and PPAR-γ protein expression.
Conclusions:
- Luteolin effectively ameliorates HFD-induced MAFLD in rats.
- Luteolin's therapeutic effects involve reducing metabolic disturbances and oxidative stress.
- Restoration of AdipoR1, AMPK, and PPAR-γ pathways is a key mechanism for luteolin's action in MAFLD.

