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Open AccessArticle

Desaturase Activity and the Risk of Type 2 Diabetes and Coronary Artery Disease: A Mendelian Randomization Study

1
Department of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, 14558 Nuthetal, Germany
2
German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany
3
Human Genomics Research Group, Department of Biomedicine, University of Basel, 4031 Basel, Switzerland
4
Institute of Human Genetics, University of Bonn, School of Medicine & University Hospital Bonn, 53105 Bonn, Germany
5
Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA
6
Institute of Nutritional Science, University of Potsdam, 14558 Nuthetal, Germany
*
Author to whom correspondence should be addressed.
Nutrients 2020, 12(8), 2261; https://doi.org/10.3390/nu12082261
Received: 10 June 2020 / Revised: 23 July 2020 / Accepted: 25 July 2020 / Published: 28 July 2020
(This article belongs to the Section Nutrition and Metabolism)
Estimated Δ5-desaturase (D5D) and Δ6-desaturase (D6D) are key enzymes in metabolism of polyunsaturated fatty acids (PUFA) and have been associated with cardiometabolic risk; however, causality needs to be clarified. We applied two-sample Mendelian randomization (MR) approach using a representative sub-cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC)–Potsdam Study and public data from DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) and Coronary ARtery DIsease Genome wide Replication and Meta-analysis (CARDIoGRAM) genome-wide association studies (GWAS). Furthermore, we addressed confounding by linkage disequilibrium (LD) as all instruments from FADS1 (encoding D5D) are in LD with FADS2 (encoding D6D) variants. Our univariable MRs revealed risk-increasing total effects of both, D6D and D5D on type 2 diabetes (T2DM) risk; and risk-increasing total effect of D6D on risk of coronary artery disease (CAD). The multivariable MR approach could not unambiguously allocate a direct causal effect to either of the individual desaturases. Our results suggest that D6D is causally linked to cardiometabolic risk, which is likely due to downstream production of fatty acids and products resulting from high D6D activity. For D5D, we found indication for causal effects on T2DM and CAD, which could, however, still be confounded by LD. View Full-Text
Keywords: Δ5-desaturase; Δ6-desaturase; type 2 diabetes; coronary artery disease; Mendelian randomization; multivariable Mendelian randomization; FADS-gene-cluster; fatty acids Δ5-desaturase; Δ6-desaturase; type 2 diabetes; coronary artery disease; Mendelian randomization; multivariable Mendelian randomization; FADS-gene-cluster; fatty acids
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MDPI and ACS Style

Jäger, S.; Cuadrat, R.; Hoffmann, P.; Wittenbecher, C.; Schulze, M.B. Desaturase Activity and the Risk of Type 2 Diabetes and Coronary Artery Disease: A Mendelian Randomization Study. Nutrients 2020, 12, 2261. https://doi.org/10.3390/nu12082261

AMA Style

Jäger S, Cuadrat R, Hoffmann P, Wittenbecher C, Schulze MB. Desaturase Activity and the Risk of Type 2 Diabetes and Coronary Artery Disease: A Mendelian Randomization Study. Nutrients. 2020; 12(8):2261. https://doi.org/10.3390/nu12082261

Chicago/Turabian Style

Jäger, Susanne; Cuadrat, Rafael; Hoffmann, Per; Wittenbecher, Clemens; Schulze, Matthias B. 2020. "Desaturase Activity and the Risk of Type 2 Diabetes and Coronary Artery Disease: A Mendelian Randomization Study" Nutrients 12, no. 8: 2261. https://doi.org/10.3390/nu12082261

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