Oxidative stress in metabolic dysfunction-associated steatotic liver disease (MASLD): How does the animal model resemble human disease?

antioxidant defense system mitochondrial respiratory chain obese patients oxidative damage reactive oxygen species

Journal

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484

Informations de publication

Date de publication:
15 Feb 2024
Historique:
revised: 15 01 2024
received: 28 11 2023
accepted: 22 01 2024
medline: 6 2 2024
pubmed: 6 2 2024
entrez: 6 2 2024
Statut: ppublish

Résumé

Despite decades of research, the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) is still not completely understood. Based on the evidence from preclinical models, one of the factors proposed as a main driver of disease development is oxidative stress. This study aimed to search for the resemblance between the profiles of oxidative stress and antioxidant defense in the animal model of MASLD and the group of MASLD patients. C57BL/6J mice were fed with the Western diet for up to 24 weeks and served as the animal model of MASLD. The antioxidant profile of mice hepatic tissue was determined by liquid chromatography-MS3 spectrometry (LC-MS/MS). The human cohort consisted of 20 patients, who underwent bariatric surgery, and 6 controls. Based on histological analysis, 4 bariatric patients did not have liver steatosis and as such were also classified as controls. Total antioxidant activity was measured in sera and liver biopsy samples. The hepatic levels of antioxidant enzymes and oxidative damage were determined by Western Blot. The levels of antioxidant enzymes were significantly altered in the hepatic tissue of mice with MASLD. In contrast, there were no significant changes in the antioxidant profile of hepatic tissue of MASLD patients, except for the decreased level of carbonylated proteins. Decreased protein carbonylation together with significant correlations between the thioredoxin system and parameters describing metabolic health suggest alterations in the thiol-redox signaling. Altogether, these data show that even though the phenotype of mice closely resembles human MASLD, the animal-to-human translation of cellular and molecular processes such as oxidative stress may be more challenging.

Identifiants

pubmed: 38318780
doi: 10.1096/fj.202302447R
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e23466

Subventions

Organisme : Fondazione AIRC per la ricerca sul cancro ETS (AIRC)
ID : AIRC,IG-23670
Organisme : Ministero dell'Università e della Ricerca (MUR)
ID : PRIN,2017 E5L5P3
Organisme : EC | HORIZON EUROPE Framework Programme (Horizon Europe)
ID : 101080329
Organisme : Narodowe Centrum Nauki (NCN)
ID : UMO-2021/43/I/NZ3/00510
Organisme : Narodowe Centrum Nauki (NCN)
ID : UMO-2018/29/B/NZ1/00589

Informations de copyright

© 2024 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.

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Auteurs

Patrycja Jakubek (P)

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Piotr Kalinowski (P)

Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland.

Agnieszka Karkucinska-Wieckowska (A)

Department of Pathology, The Children's Memorial Health Institute, Warsaw, Poland.

Aakruti Kaikini (A)

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Inês C M Simões (ICM)

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Yaiza Potes (Y)

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Beata Kruk (B)

Laboratory of Metabolic Liver Diseases, Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

Wieslawa Grajkowska (W)

Department of Pathology, The Children's Memorial Health Institute, Warsaw, Poland.

Paolo Pinton (P)

Department of Medical Sciences, Section of Experimental Medicine, Laboratory for Technologies of Advanced Therapies, University of Ferrara, Ferrara, Italy.

Piotr Milkiewicz (P)

Liver and Internal Medicine Unit, Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland.
Translational Medicine Group, Pomeranian Medical University, Szczecin, Poland.

Michał Grąt (M)

Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland.

Maciej Pronicki (M)

Department of Pathology, The Children's Memorial Health Institute, Warsaw, Poland.

Magdalena Lebiedzinska-Arciszewska (M)

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Marcin Krawczyk (M)

Laboratory of Metabolic Liver Diseases, Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
Department of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.

Mariusz R Wieckowski (MR)

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.

Classifications MeSH