A Beneficial Role for Gluteofemoral Adipose Tissue in Cerebrovascular Disease
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Le résumé fourni par la source
BACKGROUND AND OBJECTIVES: Previous studies have shown that increased body fat is associated with stroke risk, with evidence suggesting that body fat distribution, rather than total body fat, exerts a more prominent role in cerebrovascular risk prediction. In this study, we explore causal associations between body mass index (BMI)-independent adipose tissue distribution profiles and cerebrovascular disease (CVD) risk, aiming to refine the association between body fat distribution and stroke. METHODS: We selected variants associated with BMI-independent visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue (ASAT), and gluteofemoral adipose tissue (GFAT) volumes in UK Biobank, and performed univariable and multivariable Mendelian randomization (MR) analyses with ischemic stroke (IS) and subtypes (large artery stroke [LAS], cardioembolic stroke [CES], and small vessel stroke [SVS]). We used coronary artery disease (CAD), carotid intima media thickness (cIMT), and MRI-confirmed lacunar stroke as positive controls. We explored the mediatory role of common cardiovascular (systolic blood pressure, diabetes, and low-density lipoprotein), insulin resistance, inflammatory (C-reactive protein), and adipose tissue-specific (adiponectin, leptin) factors by performing 2-step mediation MR analyses. Estimates were expressed per standard deviation increase in adjusted adipose tissue volume. RESULTS: Genetic predisposition to higher GFAT volume was associated with lower risk of IS (odds ratio [OR] 0.92, 95% CI 0.86-0.98), LAS (OR 0.80, 95% CI 0.66-0.96), and SVS (OR 0.77, 95% CI 0.67-0.88), but not CES, consistent in multivariable analyses. Genetic predisposition to higher GFAT volume was also associated with lower risk of CAD (OR 0.82, 95% CI 0.76-0.88), lacunar stroke (OR 0.78, 95% CI 0.67-0.92), and mean cIMT (β = -0.073, 95% CI -0.114 to -0.031). Associations were largely consistent in sensitivity analyses. No association was observed between genetic predisposition to ASAT or VAT and IS risk. Although common vascular risk factors were the predominant mediators in the GFAT-CVD axis, adiponectin and leptin mediated a proportion of IS and CAD risk (∼15% (1.8%-57%) and ∼4.6% (0.8%-13.5%) mediated by adiponectin, respectively). DISCUSSION: This study supports a protective role of gluteofemorally distributed fat volume in CVD risk. Although this role is predominantly mediated by common vascular risk factor modification, adipose tissue-specific factors may exert a mediatory effect, suggesting a possible novel target for attenuating adiposity-related CVD risk.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- A Beneficial Role for Gluteofemoral Adipose Tissue in Cerebrovascular Disease
- Date Crossref
- 13/05/2025
- Éditeur
- Ovid Technologies (Wolters Kluwer Health)
- 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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Medical University of South Carolina Department of Neurology pays non établi dans la noticeUniversité ou école supérieure
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Broad Institute Program in Medical and Population Genetics pays non établi dans la noticeOrganisation à but non lucratif
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Institut für Schlaganfall- und Demenzforschung pays non établi dans la noticeUniversité ou école supérieure
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Ludwig-Maximilians-Universität München pays non établi dans la noticeUniversité ou école supérieure
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Brigham and Women's Hospital Department of Neurology pays non établi dans la noticeÉtablissement de santé
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Massachusetts General Hospital Center for Genomic Medicine pays non établi dans la noticeÉtablissement de santé
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Harvard University pays non établi dans la noticeUniversité ou école supérieure
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Ludwig-Maximilians-University (LMU) Hospital Institute for Stroke and Dementia Research (ISD) pays non établi dans la noticeUniversité ou école supérieure
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University Hospital of LMU Munich Institute for Stroke and Dementia Research pays non établi dans la noticeUniversité ou école supérieure
Department of Neurology — Medical University of South Carolina, Program in Medical and Population Genetics — Broad Institute et Institut für Schlaganfall- und Demenzforschung, avec 6 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.