The gut-liver axis in progressive steatotic liver disease

The gut-liver axis regulates metabolic homeostasis, with bile acids (BAs) serving as key signalling molecules. BA dysregulation is implicated in metabolic dysfunction-associated steatotic liver disease (MASLD)and metabolic dysfunction- and alcohol-associated liver disease (MetALD), yet consistent id...

Full description

Bibliographic Details
Authors: Louca, Panayiotis, Pericàs, Juan M.|||0000-0002-3645-3293, Lin, Yu, Kouraki, Afroditi, Estévez-Vázquez, Olga, Martínez-Gómez, María, Cusidó, M. Serra, Simpson, Joanna P., Cubero, Francisco Javier, Homer, Natalie Z.M., Valdes, Ana M., Menni, Cristina
Format: article
Publication Date:2025
Country:España
Institution:Universitat Autònoma de Barcelona
Repository:Dipòsit Digital de Documents de la UAB
Language:English
OAI Identifier:oai:ddd.uab.cat:320308
Online Access:https://ddd.uab.cat/record/320308
https://dx.doi.org/urn:doi:10.1016/j.jnha.2025.100671
Access Level:Open access
Keyword:Bile acids
Gut-liver axis
Liver disease
Gut microbiome
Metabolomics
Description
Summary:The gut-liver axis regulates metabolic homeostasis, with bile acids (BAs) serving as key signalling molecules. BA dysregulation is implicated in metabolic dysfunction-associated steatotic liver disease (MASLD)and metabolic dysfunction- and alcohol-associated liver disease (MetALD), yet consistent identification of BA markers and their mechanistic roles across different stages of these diseases remain elusive. Methods: We integrated three complementary studies to examine BA dysregulation: a population-based cohort (1522 females from TwinsUK with serum BA and liver biomarker data), a clinical cohort (30 patients with steatotic liver disease, fibrosis stages F0-F4, and 4 controls), and rodent models (20 rats with MASLD/MetALD vs.9 controls). BA profiles were quantified via LC-MS. Results: The primary bile acid taurocholate was consistently correlated with liver pathology: in TwinsUK, it associated with ALT (β [95%CI] 1.81 [1.27, 2.36], FDR < 0.05) both overall and when stratifying for age (<65 years, n = 923; ≥65 years, n = 599); in the clinical cohort, it was associated with F3 fibrosis (OR [95%CI] 8.56 × 10 10 [3.80 × 10 13, 1.93 × 10 6], FDR < 0.05); and in rodents, it was associated with MASLD/MetALD (OR [95%CI] 2.86 [1.17, 9.51], FDR < 0.05). The secondary bile acid taurochenodeoxycholate was associated with both early (F0, OR [95%CI] 13.63 [1.04, 179.17], p < 0.05) and advanced stages of disease (rodents, OR [95% CI] 15.41 [2.94, 311.82], FDR < 0.05).Conclusion: Taurocholate and taurochenodeoxycholate emerge as consistent BA markers across liver disease stages, suggesting BA metabolism as potential therapeutic targets. This multi-model study bridges knowledge gaps in BA-driven mechanisms, informing personalised strategies for SLD management.