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Involvement of the Gut Microbes Romboutsia hominis and Akkermansia muciniphila in the Pathophysiology and Development of Nonalcoholic Steatohepatitis

ABSTRACT: Background Nonalcoholic steatohepatitis (NASH) represents a growing global health challenge due to its propensity to progress to irreversible hepatic disorders, including fibrosis, cirrhosis, and carcinoma. This study aimed to investigate the role of gut microbiota in the pathogenesis of NASH. We have established a NASH murine model that closely mimics NASH pathophysiology using a high-fat, marginal methionine-supplemented, choline-deficient (HMF) diet. Results Through this model, we identified Romboutsia hominis as a key contributor to NASH progression, exacerbating hepatic lipid accumulation and inflammation via the tumor necrosis factor-α (TNF-α) signaling pathway. Conversely, Akkermansia muciniphila and its extracellular vesicles (EVs) mitigated NASH by reducing hepatic lipid deposition through lipid biosynthesis-related genes downregulation. Furthermore, by integrating gut microbiota profiles and serum biomarkers using a machine learning approach, we achieved over 90% accuracy in noninvasive NASH diagnosis. Conclusions These findings elucidate critical mechanisms within the gut–liver axis and suggest novel therapeutic and diagnostic strategies targeting gut microbiota for NASH.

INSTRUMENT(S): Gas Chromatography MS -

PROVIDER: MTBLS12631 | MetaboLights | 2025-06-23

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS12631_GC-MS___metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS12631_GC-MS___metabolite_profiling_v2_maf.tsv	Tabular
	s_MTBLS12631.txt	Txt

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Project description:The pathological progression of nonalcoholic fatty liver disease (NAFLD) is driven by multiple factors, and nonalcoholic steatohepatitis (NASH) represents its progressive form. In our previous studies, we found that bicyclol had beneficial effects on NAFLD/NASH. Here we aim to investigate the underlying molecular mechanisms of the bicyclol effect on NAFLD/NASH induced by high-fat diet (HFD) feeding. A mice model of NAFLD/NASH induced by HFD-feeding for 8 weeks was used. As a pretreatment, bicyclol (200 mg/kg) was given to mice by oral gavage twice daily. Hematoxylin and eosin (H&E) stains were processed to evaluate hepatic steatosis, and hepatic fibrous hyperplasia was assessed by Masson staining. Biochemistry analyses were used to measure serum aminotransferase, serum lipids, and lipids in liver tissues. Proteomics and bioinformatics analyses were performed to identify the signaling pathways and target proteins. The real-time RT-PCR and Western blot analyses were performed to verify the proteomics data. As a result, bicyclol had a markedly protective effect against NAFLD/NASH by suppressing the increase of serum aminotransferase, hepatic lipid accumulation and alleviating histopathological changes in liver tissues. Proteomics analyses showed that bicyclol remarkably restored major pathways related to immunological responses and metabolic processes altered by HFD feeding. Consistent with our previous results, bicyclol significantly inhibited inflammation and oxidative stress pathway related indexes (SAA1, GSTM1 and RDH11). Furthermore, the beneficial effects of bicyclol were closely associated with the signaling pathways of bile acid metabolism (NPC1, SLCOLA4 and UGT1A1), cytochrome P450-mediated metabolism (CYP2C54, CYP2C70 and CYP3A25), biological processes such as metal ion metabolism (Ceruloplasmin and Metallothionein-1), angiogenesis (ALDH1A1) and immunological responses (IFI204 and IFIT3). These findings suggested that bicyclol is a potential preventive agent for NAFLD/NASH by targeting multiple mechanisms in future clinical investigations.

Dataset Information

Involvement of the Gut Microbes Romboutsia hominis and Akkermansia muciniphila in the Pathophysiology and Development of Nonalcoholic Steatohepatitis

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