Effects of Melatonin and Akkermansia muciniphila on the Gut-Liver Axis in a MASLD-Associated Liver Fibrosis Model: An Integrative Multi-Omic Approach

[EN] Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of chronic liver disease worldwide. Fibrosis is the main prognostic factor and the last reversible stage before cirrhosis, yet therapeutic options remain limited. Given the strong contribution of gut dysbi...

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Detalles Bibliográficos
Autores: González Robles, Alba María, San Miguel de Vega, Beatriz, Román Sagüillo, Sara Selva de, Juárez Fernández, María, Mauriz Gutiérrez, José Luis, Martínez Flórez, Susana, Nistal González, Maria Esther, García Mediavilla, María Victoria, Sánchez Campos, Sonia
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2026
País:España
Institución:Universidad de León
Repositorio:BULERIA. Repositorio Institucional de la Universidad de León
OAI Identifier:oai:dnet:buleria_____::e4c45a0b79235654328394de3df98d2f
Acceso en línea:https://www.mdpi.com/2076-3921/15/3/306
https://hdl.handle.net/10612/28445
Access Level:acceso abierto
Palabra clave:Fisiología
Veterinaria
Gut microbiota
Akkermansia muciniphila
Melatonin
Liver fibrosis
MASLD
3109 Ciencias Veterinarias
3109.09 Fisiología
Descripción
Sumario:[EN] Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of chronic liver disease worldwide. Fibrosis is the main prognostic factor and the last reversible stage before cirrhosis, yet therapeutic options remain limited. Given the strong contribution of gut dysbiosis to MASLD progression, strategies targeting the gut microbiota are of growing interest. This study aims to evaluate the effect of melatonin, a well-known antioxidant, anti-inflammatory and antifibrotic compound, and Akkermansia muciniphila, a next-generation probiotic, on an MASLD-associated liver fibrosis model. Eight-week-old C57BL/6J mice were fed a control or Western diet supplemented with fructose and intraperitoneal CCl4 to induce liver fibrosis. After eight weeks, the animals received either no intervention, melatonin, A. muciniphila, or both for four weeks. Serum biochemistry, liver histology and gut and liver gene expression were evaluated and multi-omic analyses were performed, including gut microbiota profiling and faecal metabolomics. Statistical analyses assessed intergroup differences and correlations across datasets. Both interventions partially restored gut microbiota composition and functionality and modulated hepatic and intestinal gene expression. Melatonin and A. muciniphila exerted protective effects against MASLD-associated fibrosis, which supports their potential as adjunctive therapeutic strategies to mitigate liver injury through modulation of the gut–liver axis