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dc.contributor.authorGusarova, Viktoria
dc.contributor.authorO'Dushlaine, Colm
dc.contributor.authorTeslovich, Tanya M.
dc.contributor.authorBenotti, Peter N.
dc.contributor.authorMirshahi, Tooraj
dc.contributor.authorGottesman, Omri
dc.contributor.authorvan Hout, Cristopher V.
dc.contributor.authorMurray, Michael F.
dc.contributor.authorMahajan, Anubha
dc.contributor.authorNielsen, Jonas B.
dc.contributor.authorFritsche, Lars
dc.contributor.authorWulff, Anders Berg
dc.contributor.authorGudbjartsson, Daníel Fannar
dc.contributor.authorSjögren, Marketa
dc.contributor.authorEmdin, Connor A.
dc.contributor.authorScott, Robert A.
dc.contributor.authorLee, Wen-Jane
dc.contributor.authorSmall, Aeron
dc.contributor.authorKwee, Lydia C.
dc.contributor.authorDwivedi, Om Prakash
dc.contributor.authorPrasad, Rashmi B.
dc.contributor.authorBruse, Shannon
dc.contributor.authorLopez, Alexander E.
dc.contributor.authorPenn, John
dc.contributor.authorMarcketta, Anthony
dc.contributor.authorLeader, Joseph B.
dc.contributor.authorStill, Christopher D.
dc.contributor.authorKirchner, H. Lester
dc.contributor.authorMirshahi, Uyenlinh L.
dc.contributor.authorWardeh, Amr H.
dc.contributor.authorHartle, Cassandra M.
dc.contributor.authorHabegger, Lukas
dc.contributor.authorFetterolf, Samantha N.
dc.contributor.authorTusie-Luna, Teresa
dc.contributor.authorMorris, Andrew P.
dc.contributor.authorHolm, Hilma
dc.contributor.authorSteinthorsdóttir, Valgerdur
dc.contributor.authorSulem, Patrick
dc.contributor.authorThorsteinsdóttir, Unnur
dc.contributor.authorRotter, Jerome I.
dc.contributor.authorChuang, Lee-Ming
dc.contributor.authorDamrauer, Scott
dc.contributor.authorBirtwell, David
dc.contributor.authorBrummett, Chad M.
dc.contributor.authorKhera, Amit V.
dc.contributor.authorNatarajan, Pradeep
dc.contributor.authorOrho-Melander, Marju
dc.contributor.authorFlannick, Jason
dc.contributor.authorLotta, Luca A.
dc.contributor.authorWiller, Cristen J.
dc.contributor.authorHolmen, Oddgeir Lingaas
dc.contributor.authorRitchie, Marylyn D.
dc.contributor.authorLedbetter, David H.
dc.contributor.authorMurphy, Andrew J.
dc.contributor.authorBorecki, Ingrid B.
dc.contributor.authorReid, Jeffrey G.
dc.contributor.authorOverton, John D.
dc.contributor.authorHansson, Ola
dc.contributor.authorGroop, Leif
dc.contributor.authorShah, Svati H.
dc.contributor.authorKraus, William E.
dc.contributor.authorRader, Daniel J.
dc.contributor.authorChen, Yii-Der Ida
dc.contributor.authorHveem, Kristian
dc.contributor.authorWareham, Nicholas J.
dc.contributor.authorKathiresan, Sekar
dc.contributor.authorMelander, Olle
dc.contributor.authorStefansson, Kari
dc.contributor.authorNordestgaard, Børge G.
dc.contributor.authorTybjærg-Hansen, Anne
dc.contributor.authorAbecasis, Goncalo
dc.contributor.authorAltshuler, David
dc.contributor.authorFlorez, Jose C.
dc.contributor.authorBoehnke, Michael
dc.contributor.authorMcCarthy, Mark I.
dc.contributor.authorYancopoulos, George D.
dc.contributor.authorCarey, David J.
dc.contributor.authorShuldiner, Alan R.
dc.contributor.authorBaras, Aris
dc.contributor.authorDewey, Frederick E.
dc.contributor.authorGromada, Jesper
dc.identifier.citationNature Communications. 2018, 9 1-11.nb_NO
dc.description.abstractAngiopoietin-like 4 (ANGPTL4) is an endogenous inhibitor of lipoprotein lipase that modulates lipid levels, coronary atherosclerosis risk, and nutrient partitioning. We hypothesize that loss of ANGPTL4 function might improve glucose homeostasis and decrease risk of type 2 diabetes (T2D). We investigate protein-altering variants in ANGPTL4 among 58,124 participants in the DiscovEHR human genetics study, with follow-up studies in 82,766 T2D cases and 498,761 controls. Carriers of p.E40K, a variant that abolishes ANGPTL4 ability to inhibit lipoprotein lipase, have lower odds of T2D (odds ratio 0.89, 95% confidence interval 0.85–0.92, p = 6.3 × 10−10), lower fasting glucose, and greater insulin sensitivity. Predicted loss-of-function variants are associated with lower odds of T2D among 32,015 cases and 84,006 controls (odds ratio 0.71, 95% confidence interval 0.49–0.99, p = 0.041). Functional studies in Angptl4-deficient mice confirm improved insulin sensitivity and glucose homeostasis. In conclusion, genetic inactivation of ANGPTL4 is associated with improved glucose homeostasis and reduced risk of T2D.nb_NO
dc.publisherNature Researchnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleGenetic inactivation of ANGPTL4 improves glucose homeostasis and is associated with reduced risk of diabetesnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalNature Communicationsnb_NO
dc.relation.projectNorges forskningsråd: 248817nb_NO
dc.description.localcodeOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
cristin.unitnameInstitutt for samfunnsmedisin og sykepleie
cristin.unitnameHelseundersøkelsen i Nord-Trøndelag

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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal