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Contribution of genetics to visceral adiposity and its relation to cardiovascular and metabolic disease.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab. (Åsa Johansson)ORCID iD: 0000-0001-8095-6149
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab. (Åsa Johansson)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.ORCID iD: 0000-0001-8061-3947
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2019 (English)In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 25, no 9, p. 1390-1395Article in journal (Refereed) Published
Abstract [en]

Visceral adipose tissue (VAT)-fat stored around the internal organs-has been suggested as an independent risk factor for cardiovascular and metabolic disease1-3, as well as all-cause, cardiovascular-specific and cancer-specific mortality4,5. Yet, the contribution of genetics to VAT, as well as its disease-related effects, are largely unexplored due to the requirement for advanced imaging technologies to accurately measure VAT. Here, we develop sex-stratified, nonlinear prediction models (coefficient of determination = 0.76; typical 95% confidence interval (CI) = 0.74-0.78) for VAT mass using the UK Biobank cohort. We performed a genome-wide association study for predicted VAT mass and identified 102 novel visceral adiposity loci. Predicted VAT mass was associated with increased risk of hypertension, heart attack/angina, type 2 diabetes and hyperlipidemia, and Mendelian randomization analysis showed visceral fat to be a causal risk factor for all four diseases. In particular, a large difference in causal effect between the sexes was found for type 2 diabetes, with an odds ratio of 7.34 (95% CI = 4.48-12.0) in females and an odds ratio of 2.50 (95% CI = 1.98-3.14) in males. Our findings bolster the role of visceral adiposity as a potentially independent risk factor, in particular for type 2 diabetes in Caucasian females. Independent validation in other cohorts is necessary to determine whether the findings can translate to other ethnicities, or outside the UK.

Place, publisher, year, edition, pages
2019. Vol. 25, no 9, p. 1390-1395
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Medical Genetics
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URN: urn:nbn:se:uu:diva-392977DOI: 10.1038/s41591-019-0563-7ISI: 000484832800021PubMedID: 31501611OAI: oai:DiVA.org:uu-392977DiVA, id: diva2:1350739
Funder
Swedish National Infrastructure for Computing (SNIC), b2016021Swedish National Infrastructure for Computing (SNIC), sens2017538Swedish Society for Medical Research (SSMF)Swedish Research Council, 2015-03327Göran Gustafsson Foundation for Research in Natural Sciences and MedicineÅke Wiberg Foundation, M16-0210Swedish Heart Lung Foundation, 20170484Swedish Diabetes AssociationScience for Life Laboratory - a national resource center for high-throughput molecular bioscienceAvailable from: 2019-09-12 Created: 2019-09-12 Last updated: 2019-11-20Bibliographically approved

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Karlsson, TorgnyRask-Andersen, MathiasPan, GangHöglund, JuliaWadelius, ClaesEk, Weronica EJohansson, Åsa

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