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Ginsenoside F1 improves mitochondrial energy metabolism through regulating gut microbiota-induced bile acid homeostasis [RNA-Seq]

ABSTRACT: This study investigates the effects of ginsenoside F1 (GF1), a rare ginsenoside, on metabolic syndrome (MetS) in a high‑fat diet (HFD)‑induced mouse model. Male C57BL/6 mice were fed a HFD for 8 weeks to establish MetS and then treated with GF1 at 50 or 100 mg/kg/day for 12 weeks, alongside chow‑fed controls. Metabolic phenotypes were assessed via indirect calorimetry, serum biochemical assays, histopathological examination, and oral glucose tolerance tests. To elucidate the underlying mechanisms, we performed a comprehensive multi‑omics and functional analysis, including RNA‑sequencing of liver and subcutaneous white adipose tissue (sWAT), 16S rRNA gene sequencing of gut microbiota from fecal samples, targeted metabolomics for bile acid profiling in liver tissues, flow cytometry for immune cell phenotyping in blood, liver, and stromal vascular fraction of adipose tissue, as well as Western blotting and immunohistochemistry for protein validation. This dataset provides extensive transcriptomic, microbiomic, and metabolomic data to evaluate the potential mechanisms of GF1 in modulating energy metabolism, mitochondrial function, inflammation, and gut microbiota–bile acid crosstalk in the context of diet‑induced MetS.

ORGANISM(S): Mus musculus

PROVIDER: GSE342545 | GEO | 2026/08/31

REPOSITORIES: GEO

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Project description:Background: Western diet (WD) fed Melanocortin 4 receptor-knockout (MC4R-KO) mice develop a phenotype resembling human metabolic dysfunction-associated steatohepatitis (MASH). Despite its clinical relevance, the role of the gut–liver axis in MASH pathogenesis remains unclear. This study investigated the gut-liver axis through microbiomic and metabolomic analyses of WD-fed MC4R-KO mice, and examined their association with MASH pathology. Methods: We performed an integrated microbiome and metabolome analysis of the liver, small intestinal contents, large intestinal contents, and plasma of wild-type (WT) and MC4R-KO mice fed either a normal diet or WD. Markers of hepatic inflammation, fibrosis, and steatosis measured in this study were used to assess MASH severity and to correlate microbiome and metabolite alterations. Results: WD-fed MC4R-KO mice exhibited significant hepatic steatosis, inflammation, and fibrosis. The abundance of certain microbiota, including Muribaculaceae and Allobaculum, negatively correlated with MASH severity, whereas increased levels of Desulfovibrionaceae and Bacteroides positively correlated with hepatic lipid accumulation, steatosis, and inflammation. Metabolomic profiling revealed increased triglyceride and diglyceride levels in the liver and a concomitant decrease in free fatty acids and monoglycerides in the intestines. Additionally, plasma taurine-conjugated bile acids were elevated in WD-fed MC4R-KO mice, which correlated with the reduced hepatic transport of bile salts from pathway enrichment analysis. These findings highlight substantial alterations in the gut microbiota and lipid and bile acid metabolism, indicating a mechanistic dysregulation of the gut–liver axis that may contribute to MASH progression. Conclusions: The observed gut microbial and metabolic alterations, particularly bile acid and lipid metabolism dysregulation, offer insights into potential therapeutic targets aimed at modulating the gut–liver axis to treat or prevent MASH.

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Ginsenoside F1 improves mitochondrial energy metabolism through regulating gut microbiota-induced bile acid homeostasis [RNA-Seq]

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