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Fatty acids in the de novo lipogenesis pathway and incidence of type 2 diabetes: A pooled analysis of prospective cohort studies

dc.rights.licenseopenen_US
dc.contributor.authorIMAMURA, F.
dc.contributor.authorFRETTS, A. M.
dc.contributor.authorMARKLUND, M.
dc.contributor.authorARDISSON KORAT, A. V.
dc.contributor.authorYANG, W. S.
dc.contributor.authorLANKINEN, M.
dc.contributor.authorQURESHI, W.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorHELMER, Catherine
dc.contributor.authorCHEN, T. A.
dc.contributor.authorVIRTANEN, J. K.
dc.contributor.authorWONG, K.
dc.contributor.authorBASSETT, J. K.
dc.contributor.authorMURPHY, R.
dc.contributor.authorTINTLE, N.
dc.contributor.authorYU, C. I.
dc.contributor.authorBROUWER, I. A.
dc.contributor.authorCHIEN, K. L.
dc.contributor.authorCHEN, Y. Y.
dc.contributor.authorWOOD, A. C.
dc.contributor.authorDEL GOBBO, L. C.
dc.contributor.authorDJOUSSE, L.
dc.contributor.authorGELEIJNSE, J. M.
dc.contributor.authorGILES, G. G.
dc.contributor.authorDE GOEDE, J.
dc.contributor.authorGUDNASON, V.
dc.contributor.authorHARRIS, W. S.
dc.contributor.authorHODGE, A.
dc.contributor.authorHU, F.
dc.contributor.authorKOULMAN, A.
dc.contributor.authorLAAKSO, M.
dc.contributor.authorLIND, L.
dc.contributor.authorLIN, H. J.
dc.contributor.authorMCKNIGHT, B.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorRAJAOBELINA, Kalina
dc.contributor.authorRISERUS, U.
dc.contributor.authorROBINSON, J. G.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorSAMIERI, Cecilia
dc.contributor.authorSENN, M.
dc.contributor.authorSISCOVICK, D. S.
dc.contributor.authorSOEDAMAH-MUTHU, S. S.
dc.contributor.authorSOTOODEHNIA, N.
dc.contributor.authorSUN, Q.
dc.contributor.authorTSAI, M. Y.
dc.contributor.authorTUOMAINEN, T. P.
dc.contributor.authorUUSITUPA, M.
dc.contributor.authorWAGENKNECHT, L. E.
dc.contributor.authorWAREHAM, N. J.
dc.contributor.authorWU, J. H. Y.
dc.contributor.authorMICHA, R.
dc.contributor.authorLEMAITRE, R. N.
dc.contributor.authorMOZAFFARIAN, D.
dc.contributor.authorFOROUHI, N. G.
dc.date.accessioned2021-02-23T15:48:47Z
dc.date.available2021-02-23T15:48:47Z
dc.date.issued2020
dc.identifier.issn1549-1277en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/26336
dc.description.abstractEnBackground De novo lipogenesis (DNL) is the primary metabolic pathway synthesizing fatty acids from carbohydrates, protein, or alcohol. Our aim was to examine associations of in vivo levels of selected fatty acids (16:0, 16:1n7, 18:0, 18:1n9) in DNL with incidence of type 2 diabetes (T2D). Methods and findings Seventeen cohorts from 12 countries (7 from Europe, 7 from the United States, 1 from Australia, 1 from Taiwan; baseline years = 1970–1973 to 2006–2010) conducted harmonized individual-level analyses of associations of DNL-related fatty acids with incident T2D. In total, we evaluated 65,225 participants (mean ages = 52.3–75.5 years; % women = 20.4%–62.3% in 12 cohorts recruiting both sexes) and 15,383 incident cases of T2D over the 9-year follow-up on average. Cohort-specific association of each of 16:0, 16:1n7, 18:0, and 18:1n9 with incident T2D was estimated, adjusted for demographic factors, socioeconomic characteristics, alcohol, smoking, physical activity, dyslipidemia, hypertension, menopausal status, and adiposity. Cohort-specific associations were meta-analyzed with an inverse-variance-weighted approach. Each of the 4 fatty acids positively related to incident T2D. Relative risks (RRs) per cohort-specific range between midpoints of the top and bottom quintiles of fatty acid concentrations were 1.53 (1.41–1.66; p < 0.001) for 16:0, 1.40 (1.33–1.48; p < 0.001) for 16:1n-7, 1.14 (1.05–1.22; p = 0.001) for 18:0, and 1.16 (1.07–1.25; p < 0.001) for 18:1n9. Heterogeneity was seen across cohorts (I2 = 51.1%–73.1% for each fatty acid) but not explained by lipid fractions and global geographical regions. Further adjusted for triglycerides (and 16:0 when appropriate) to evaluate associations independent of overall DNL, the associations remained significant for 16:0, 16:1n7, and 18:0 but were attenuated for 18:1n9 (RR = 1.03, 95% confidence interval (CI) = 0.94–1.13). These findings had limitations in potential reverse causation and residual confounding by imprecisely measured or unmeasured factors. Conclusions Concentrations of fatty acids in the DNL were positively associated with T2D incidence. Our findings support further work to investigate a possible role of DNL and individual fatty acids in the development of T2D.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subjectLEHA
dc.title.enFatty acids in the de novo lipogenesis pathway and incidence of type 2 diabetes: A pooled analysis of prospective cohort studies
dc.title.alternativePLoS Meden_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1371/journal.pmed.1003102en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed32530938en_US
bordeaux.journalPLoS Medicineen_US
bordeaux.pagee1003102en_US
bordeaux.volume17en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219en_US
bordeaux.issue6en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.teamLEHA_BPH
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03150333
hal.version1
hal.date.transferred2021-02-23T15:48:55Z
hal.exporttrue
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