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dc.contributor.authorMurphy, Aoife M
dc.contributor.authorSmith, Caren E
dc.contributor.authorMurphy, Leanne M
dc.contributor.authorFollis, Jack L
dc.contributor.authorTanaka, Toshiko
dc.contributor.authorRichardson, Kris
dc.contributor.authorNoordam, Raymond
dc.contributor.authorLemaitre, Rozenn N
dc.contributor.authorKähönen, Mika
dc.contributor.authorDupuis, Josée
dc.contributor.authorVoortman, Trudy
dc.contributor.authorMarouli, Eirini
dc.contributor.authorMook-Kanamori, Dennis O
dc.contributor.authorRaitakari, Olli T
dc.contributor.authorHong, Jaeyoung
dc.contributor.authorDehghan, Abbas
dc.contributor.authorDedoussis, George
dc.contributor.authorde Mutsert, Renée
dc.contributor.authorLehtimäki, Terho
dc.contributor.authorLiu, Ching-Ti
dc.contributor.authorRivadeneira, Fernando
dc.contributor.authorDeloukas, Panagiotis
dc.contributor.authorMikkilä, Vera
dc.contributor.authorMeigs, James B
dc.contributor.authorUitterlinden, Andre
dc.contributor.authorIkram, Mohammad A
dc.contributor.authorFranco, Oscar H
dc.contributor.authorHughes, Maria
dc.contributor.authorO' Gaora, Peadar
dc.contributor.authorOrdovas, Jose M 
dc.contributor.authorRoche, Helen M
dc.date.accessioned2019-10-17T08:40:20Z
dc.date.available2019-10-17T08:40:20Z
dc.date.issued2019-08-20
dc.identifier.citationMol Nutr Food Res. 2019: e1900226es_ES
dc.identifier.issn1613-4125es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8505
dc.description.abstractSCOPE: Insulin resistance (IR) and inflammation are hallmarks of type 2 diabetes (T2D). The nod-like receptor pyrin domain containing-3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL-1β inflammation and IR. Interactions between SFA intake and NLRP3-related genetic variants may alter T2D risk factors. METHODS: Meta-analyses of six Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (n = 19 005) tested interactions between SFA and NLRP3-related single-nucleotide polymorphisms (SNPs) and modulation of fasting insulin, fasting glucose, and homeostasis model assessment of insulin resistance. RESULTS: SFA interacted with rs12143966, wherein each 1% increase in SFA intake increased insulin by 0.0063 IU mL-1 (SE ± 0.002, p = 0.001) per each major (G) allele copy. rs4925663, interacted with SFA (β ± SE = -0.0058 ± 0.002, p = 0.004) to increase insulin by 0.0058 IU mL-1 , per additional copy of the major (C) allele. Both associations are close to the significance threshold (p < 0.0001). rs4925663 causes a missense mutation affecting NLRP3 expression. CONCLUSION: Two NLRP3-related SNPs showed potential interaction with SFA to modulate fasting insulin. Greater dietary SFA intake accentuates T2D risk, which, subject to functional validation, may be further elaborated depending on NLRP3-related genetic variants.es_ES
dc.language.isoenges_ES
dc.publisherWiley es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/*
dc.subjectCohorts for Heart and Ageing Research in Genomic Epidemiology consortiumes_ES
dc.subjectNLRP3 inflammasomeses_ES
dc.subjectGenome-wide interaction studieses_ES
dc.subjectInsulin resistancees_ES
dc.subjectMeta-analyseses_ES
dc.subjectSaturated fatses_ES
dc.titlePotential Interplay between Dietary Saturated Fats and Genetic Variants of the NLRP3 Inflammasome to Modulate Insulin Resistance and Diabetes Risk: Insights from a Meta-Analysis of 19 005 Individualses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial 4.0 Internacional*
dc.identifier.pubmedID31432628es_ES
dc.format.pagee1900226es_ES
dc.identifier.doi10.1002/mnfr.201900226es_ES
dc.contributor.funderScience Foundation Ireland 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1613-4133es_ES
dc.relation.publisherversionhttps://doi.org/10.1002/mnfr.201900226es_ES
dc.identifier.journalMolecular nutrition & food researches_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Imagen Cardiovascular y Estudios Poblacionaleses_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsopen accesses_ES


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