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Hawthorn flavonoids ameliorate NAFLD in mice: Association with enhanced gut butyrate production and hepatic PI3K/Akt signaling activation
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DOI：10.2306/scienceasia1513-1874.2026.037.png)
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Abstract
En 中文
Gut dysbiosis and disrupted gut-liver crosstalk drive non-alcoholic fatty liver disease (NAFLD), a global health burden intertwined with obesity and insulin resistance. This study investigated the therapeutic potential of Hawthorn flavonoid extract (HF) from Crataegus species in NAFLD management, focusing on its modulation of gut microbiota and metabolic pathways. Using a high-fat diet-induced NAFLD mouse model, 12-week HF supplementation (100 mg/kg/day) was administered. We evaluated therapeutic effects via hepatic steatosis, systemic insulin resistance, antioxidant capacity (SOD, GSH-Px, and MDA), and liver histology. Mechanistic insights were gained through gut microbiota composition, fecal butyrate, hepatic PI3K/Akt activation, and serum metabolomics. HF significantly attenuated hepatic steatosis, improved insulin sensitivity (p < 0.05), and restored antioxidant capacity by elevating SOD/GSH-Px activity and suppressing lipid peroxidation (MDA). Histology confirmed reduced hepatic lipid accumulation and inflammation. Furthermore, HF favorably altered gut microbial composition, enriching beneficial genera such as Akkermansia and Bacteroides, and increased colonic butyrate production. This microbial shift correlated with hepatic PI3K/Akt pathway activation (p <0.05). Serum metabolomics identified HF-mediated reprogramming of taurine metabolism, glutathione recycling, and glycerophospholipid dynamics. In conclusion, HF alleviates NAFLD progression by restoring gut microbial ecology, enhancing butyrate production, and activating hepatic PI3K/Akt signaling, collectively modulating oxidative stress and lipid metabolism.
Keywords:
non-alcoholic fatty liver disease
Hawthorn flavonoids
butyrate
PI3K/Akt pathway
oxidative stress
gut microbiota
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