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Increased hepatic putrescine levels as a new potential factor related to the progression of metabolic dysfunction-associated steatotic liver disease.

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dc.contributor.authorNuñez-Sanchez, Maria Ángeles
dc.contributor.authorMartinez-Sanchez, María Antonia
dc.contributor.authorSierra-Cruz, Marta
dc.contributor.authorRico-Chazarra, Sara
dc.contributor.authorOliva-Bolarín, Alba
dc.contributor.authorBalaguer-Román, Andrés
dc.contributor.authorYuste, José Enrique
dc.contributor.authorMika, Adriana
dc.contributor.authorFrutos, María Dolores
dc.contributor.authorRamos-Molina, Bruno
dc.contributor.authorMartínez Cáceres, Carlos Manuel
dc.contributor.authorLambertos Escudero, Ana
dc.contributor.departmentBioquímica y Biología Molecular B e Inmunología
dc.date.accessioned2025-01-22T08:57:39Z
dc.date.available2025-01-22T08:57:39Z
dc.date.issued2024-07-18
dc.description© 2024 The Pathological Society of Great Britain and Ireland. This document is the accepted version of a published work that appeared in final form in The Journal of Pathology To access the final edited and published work see: https://doi.org/10.1002/path.6330
dc.description.abstractMetabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic liver condition that often progresses to more advanced stages, such as metabolic dysfunction-associated steatohepatitis (MASH). MASH is characterized by inflammation and hepatocellular ballooning, in addition to hepatic steatosis. Despite the relatively high incidence of MASH in the population and its potential detrimental effects on human health, this liver disease is still not fully understood from a pathophysiological perspective. Deregulation of polyamine levels has been detected in various pathological conditions, including neurodegenerative diseases, inflammation, and cancer. However, the role of the polyamine pathway in chronic liver disorders such as MASLD has not been explored. In this study, we measured the expression of liver ornithine decarboxylase (ODC1), the rate-limiting enzyme responsible for the production of putrescine, and the hepatic levels of putrescine, in a preclinical model of MASH as well as in liver biopsies of patients with obesity undergoing bariatric surgery. Our findings reveal that expression of ODC1 and the levels of putrescine, but not spermidine nor spermine, are elevated in hepatic tissue of both diet-induced MASH mice and patients with biopsy-proven MASH compared with control mice and patients without MASH, respectively. Furthermore, we found that the levels of putrescine were positively associated with higher aspartate aminotransferase concentrations in serum and an increased SAF score (steatosis, activity, fibrosis). Additionally, in in vitro assays using human HepG2 cells, we demonstrate that elevated levels of putrescine exacerbate the cellular response to palmitic acid, leading to decreased cell viability and increased release of CK-18. Our results support an association between the expression of ODC1 and the progression of MASLD, which could have translational relevance in understanding the onset of this disease. (c) 2024 The Pathological Society of Great Britain and Ireland.es
dc.formatapplication/pdfes
dc.format.extent11es
dc.identifier.citationJournal of Pathology 264 (1) 101-111
dc.identifier.doihttps://doi.org/10.1002/path.6330
dc.identifier.issnPrint.:0222-3417
dc.identifier.issnelectronic.:1096-9896
dc.identifier.urihttp://hdl.handle.net/10201/149024
dc.languageenges
dc.publisherWILEYes
dc.relationInstituto de Salud Carlos III p PI22/00404 European Union AECC Scientific Foundation POSTD235118CAST Universidad de Murcia  es
dc.relation.publisherversionhttps://pathsocjournals.onlinelibrary.wiley.com/doi/full/10.1002/path.6330
dc.rightsAttribution-NonCommercial-NoDerivates 4.0 International
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleIncreased hepatic putrescine levels as a new potential factor related to the progression of metabolic dysfunction-associated steatotic liver disease.es
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
relation.isAuthorOfPublicationa11bfbe4-fe50-4173-a96d-aa785375a6be
relation.isAuthorOfPublication5d0e7a0e-9ee6-41f7-8b88-142f6d773781
relation.isAuthorOfPublication.latestForDiscoverya11bfbe4-fe50-4173-a96d-aa785375a6be
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