What question did this study set out to answer?

This study aims to evaluate the effects of ethyl gallate on high-fat diet-induced non-alcoholic fatty liver disease in mice.

March 28, 2026Open Access

Ethyl Gallate Ameliorates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Suppressing Inflammation and Modulating the Gut Microbiota-Intestinal Barrier Axis

Key Points

This study aims to evaluate the effects of ethyl gallate on high-fat diet-induced non-alcoholic fatty liver disease in mice.
Used a high-fat diet (HFD) mouse model for 12 weeks.
Administered ethyl gallate (10 or 20 mg/kg) from week 3 to week 12.
Analyzed through histopathology, serum biochemical analysis, and cytokine measurements.
Performed 16S rRNA gene sequencing for gut microbiota analysis.
Evaluated tight junction proteins to assess intestinal barrier function.
Ethyl gallate significantly reduced hepatic steatosis and improved serum lipid profiles.
Enhanced glucose tolerance and insulin sensitivity were observed in treated mice.
The treatment led to lower levels of pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α.
Ethyl gallate restored gut microbiota diversity and corrected dysbiosis caused by HFD.
Increased levels of tight junction proteins improved intestinal barrier integrity.

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder with rising global prevalence, yet effective therapeutic options remain limited. Chronic inflammation and gut microbiota dysbiosis are key contributors to NAFLD progression. Ethyl gallate (EG), a natural polyphenolic compound, exhibits anti-inflammatory and antioxidant properties. However, its therapeutic potential and underlying mechanisms in NAFLD remain unclear. This study aimed to evaluate the effects of EG in a high-fat diet (HFD)-induced NAFLD mouse model. Mice were fed an HFD for 12 weeks, with EG administered (10 or 20 mg/kg) from week 3 to week 12. The impact of EG was assessed through histopathological examination, serum biochemical analysis, glucose tolerance and insulin sensitivity tests, hepatic and systemic pro-inflammatory cytokine measurements, 16 S rRNA gene sequencing and intestinal tight junction protein evaluation. EG treatment markedly alleviated hepatic steatosis, improved serum lipid profiles, and enhanced glucose tolerance and insulin sensitivity. Moreover, EG significantly reduced hepatic and systemic levels of pro-inflammatory cytokines, including IL-1β, IL-6 and TNF-α. Gut microbiota analysis revealed that EG reversed HFD-induced increases in Firmicutes and Actinobacteria and the reduction in Bacteroidetes, partially restoring microbial diversity. Notably, EG suppressed the overgrowth of Faecalibaculum and Dubosiella while restoring Ligilactobacillus and Alistipes abundance. Furthermore, EG enhanced intestinal barrier integrity by upregulating tight junction proteins Claudin-1, Occludin and ZO-1, thereby reducing endotoxin translocation. Collectively, EG effectively ameliorates HFD-induced NAFLD by suppressing inflammation, modulating gut microbiota composition, and reinforcing intestinal barrier function. These findings highlight the potential of EG as a promising therapeutic candidate for the prevention and treatment of NAFLD.

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