The impact of steatotic liver disease on coronary artery disease through changes in the plasma lipidome.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
27 Sep 2024
Historique:
received: 08 02 2024
accepted: 17 09 2024
medline: 28 9 2024
pubmed: 28 9 2024
entrez: 27 9 2024
Statut: epublish

Résumé

Steatotic liver disease has been shown to associate with cardiovascular disease independently of other risk factors. Lipoproteins have been shown to mediate some of this relationship but there remains unexplained variance. Here we investigate the plasma lipidomic changes associated with liver steatosis and the mediating effect of these lipids on coronary artery disease (CAD). In a population of 2579 Swedish participants of ages 50 to 65 years, lipids were measured by mass spectrometry, liver fat was measured using computed tomography (CT), and CAD status was defined as the presence of coronary artery calcification (CAC score > 0). Lipids associated with liver steatosis and CAD were identified and their mediating effects between the two conditions were investigated. Out of 458 lipids, 284 were found to associate with liver steatosis and 19 of them were found to also associate with CAD. Two fatty acids, docosatrienoate (22:3n6) and 2-hydroxyarachidate, presented the highest mediating effect between steatotic liver disease and CAD. Other mediators were also identified among sphingolipids and glycerophospholipids, although their mediating effects were attenuated when adjusting for circulating lipoproteins. Further research should investigate the role of docosatrienoate (22:3n6) and 2-hydroxyarachidate as mediators between steatotic liver disease and CAD alongside known risk factors.

Identifiants

pubmed: 39333359
doi: 10.1038/s41598-024-73406-8
pii: 10.1038/s41598-024-73406-8
doi:

Substances chimiques

Lipids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

22307

Informations de copyright

© 2024. The Author(s).

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Auteurs

Elias Björnson (E)

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, Gothenburg, 413 45, Sweden. elias.bjornson@wlab.gu.se.

Dimitrios Samaras (D)

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, Gothenburg, 413 45, Sweden.

Malin Levin (M)

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, Gothenburg, 413 45, Sweden.

Fredrik Bäckhed (F)

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, Gothenburg, 413 45, Sweden.
Region Västra Götaland, Department of Clinical Physiology, Sahlgrenska University Hospital, Gothenburg, 41345, Sweden.

Göran Bergström (G)

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, Gothenburg, 413 45, Sweden.
Region Västra Götaland, Department of Clinical Physiology, Sahlgrenska University Hospital, Gothenburg, 41345, Sweden.

Anders Gummesson (A)

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Center for Cardiovascular and Metabolic Research, University of Gothenburg, Gothenburg, 413 45, Sweden.
Region Västra Götaland, Department of Clinical Genetics, Sahlgrenska University Hospital, Gothenburg, 413 45, Sweden.

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