Author response: A Host Enzyme Reduces Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) by Inactivating Intestinal Lipopolysaccharide
Rattachement africain : cn, us. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
The incidence of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) has been increasing world-wide. Since gut-derived bacterial lipopolysaccharides (LPS) can travel via the portal vein to the liver and play an important role in producing hepatic pathology, it seemed possible that (1) LPS stimulates hepatic cells to accumulate lipid, and (2) inactivating LPS can be preventive. Acyloxyacyl hydrolase (AOAH), the eukaryotic lipase that inactivates LPS and oxidized phospholipids, is produced in the intestine, liver, and other organs. We fed mice either normal chow or a high-fat diet for 28 weeks and found that Aoah−/− mice accumulated more hepatic lipid than did Aoah+/+ mice. In young mice, before increased hepatic fat accumulation was observed, Aoah−/−mouse livers increased their abundance of Sterol Regulatory Element-Binding Protein 1 (SREBP1) and the expression of its target genes that promote fatty acid synthesis. Aoah−/− mice also increased hepatic expression of CD36 and Fabp3, which mediate fatty acid uptake, and decreased expression of fatty acid oxidation-related genes Acot2 and Ppar-α. Our results provide evidence that increasing AOAH abundance in the gut, bloodstream and/or liver may be an effective strategy for preventing or treating MASLD.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Author response: A Host Enzyme Reduces Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) by Inactivating Intestinal Lipopolysaccharide
- Date Crossref
- 09/04/2025
- Éditeur
- eLife Sciences Publications, Ltd
- Type
- peer-review
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Fudan University Department of Gastroenterology pays non établi dans la noticeUniversité ou école supérieure
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The University of Texas Southwestern Medical Center Department of Internal Medicine pays non établi dans la noticeÉtablissement de santé
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Affiliated Hospital of Guizhou Medical University Department of Rheumatology and Immunology pays non établi dans la noticeÉtablissement de santé
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BeiGene (China) pays non établi dans la noticeEntreprise
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National Institutes of Health pays non établi dans la noticeOrganisme public
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National Institute of Allergy and Infectious Diseases pays non établi dans la noticeStructure de recherche
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School of Basic Medical Sciences Department of Immunology pays non établi dans la noticeUniversité ou école supérieure
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BeiGene Institute pays non établi dans la noticeStructure de recherche
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Laboratory of Clinical Immunology and Microbiology Antibacterial Host Defense Unit pays non établi dans la noticeStructure de recherche
Department of Gastroenterology — Fudan University, Department of Internal Medicine — The University of Texas Southwestern Medical Center et Department of Rheumatology and Immunology — Affiliated Hospital of Guizhou Medical University, avec 6 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.