Distinct metabolic perturbations link liver steatosis and incident CVD in lean but not obese PWH
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Le résumé fourni par la source
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a key risk factor for cardiovascular disease (CVD), potentially driven by shared metabolic mechanisms. Metabolic perturbations associated with MASLD and CVD remain underexplored in people with HIV (PWH). METHODS: We used data from the longitudinal multicenter 2000HIV study comprising 1895 virally suppressed PWH, out of which 970 had available liver and carotid artery measurements. Transient elastography with controlled attenuation parameter (CAP) was performed for the assessment of liver steatosis (CAP > 263 dB/m) and fibrosis (LSM ≥ 7.0). Historic and future incident CVD within 2-year follow-up, defined as myocardial infarction, stroke, peripheral arterial disease, and angina pectoris, were extracted from the medical files, while atherosclerotic plaque(s) in the carotid arteries were assessed using ultrasonography. Metabolic perturbations were analyzed using mass spectrometry-based untargeted metabolomics (n = 500 metabolites) and nuclear magnetic resonance spectroscopy for targeted lipids and other metabolites (n = 246 metabolites). RESULTS: . Metabolic pathways associated with liver steatosis and fibrosis primarily involved lipid and amino acid metabolism, and they were validated by targeted lipoproteomic measurements. Interestingly, metabolomic pathways and lipoproteomic signatures associated with MASLD were mostly distinct from those associated with CVD parameters. However, several metabolic pathways were shared, especially in lean PWH. These include arachidonic acid metabolism and formation of prostaglandin, purine metabolism, cholecalciferol metabolism, and glycine, serine, alanine, and threonine metabolism. CONCLUSION: Metabolic disturbances linked to liver steatosis and CVD diverge across BMI categories in PWH. Lean PWH, unlike their overweight/obese counterparts, show common metabolic perturbations between MASLD and CVD, particularly involving arachidonic acid metabolism. This suggests that lean PWH with liver steatosis may face a heightened risk of CVD due to shared metabolic pathways, potentially opening avenues for targeted interventions, such as aspirin therapy, to mitigate this risk.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Distinct metabolic perturbations link liver steatosis and incident CVD in lean but not obese PWH
- Date Crossref
- 11/02/2025
- Éditeur
- Springer Science and Business Media LLC
- Type
- journal-article
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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Radboud University Nijmegen pays non établi dans la noticeUniversité ou école supérieure
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Radboud University Medical Center pays non établi dans la noticeOrganisme public
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Radboud Institute for Molecular Life Sciences pays non établi dans la noticeStructure de recherche
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Rumah Sakit Umum Pusat Nasional Dr. Cipto Mangunkusumo pays non établi dans la noticeÉtablissement de santé
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Elisabeth-TweeSteden Ziekenhuis pays non établi dans la noticeÉtablissement de santé
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Erasmus MC pays non établi dans la noticeÉtablissement de santé
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OLVG pays non établi dans la noticeÉtablissement de santé
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University of Indonesia pays non établi dans la noticeUniversité ou école supérieure
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University of Bonn Department of Metabolism and Immunology pays non établi dans la noticeUniversité ou école supérieure
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Life & Brain (Germany) pays non établi dans la noticeEntreprise
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Iuliu Hațieganu University of Medicine and Pharmacy Department of Medical Genetics pays non établi dans la noticeUniversité ou école supérieure
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Department of Internal Medicine pays non établi dans la noticeInstitution
Radboud University Nijmegen, Radboud University Medical Center et Radboud Institute for Molecular Life Sciences, avec 9 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.