Sökning: WFRF:(Paananen A) > A Genome-Wide Assoc...
Fältnamn | Indikatorer | Metadata |
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000 | 05336naa a2201081 4500 | |
001 | oai:gup.ub.gu.se/255727 | |
003 | SwePub | |
008 | 240528s2017 | |||||||||||000 ||eng| | |
024 | 7 | a https://gup.ub.gu.se/publication/2557272 URI |
024 | 7 | a https://doi.org/10.2337/db16-14522 DOI |
040 | a (SwePub)gu | |
041 | a eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Wood, A. R.4 aut |
245 | 1 0 | a A Genome-Wide Association Study of IVGTT-Based Measures of First-Phase Insulin Secretion Refines the Underlying Physiology of Type 2 Diabetes Variants |
264 | c 2017-05-10 | |
264 | 1 | b American Diabetes Association,c 2017 |
520 | a Understanding the physiological mechanisms by which common variants predispose to type 2 diabetes requires large studies with detailed measures of insulin secretion and sensitivity. Here we performed the largest genome-wide association study of first-phase insulin secretion, as measured by intravenous glucose tolerance tests, using up to 5,567 individuals without diabetes from 10 studies. We aimed to refine the mechanisms of 178 known associations between common variants and glycemic traits and identify new loci. Thirty type 2 diabetes or fasting glucose-raising alleles were associated with a measure of first-phase insulin secretion at P < 0.05 and provided new evidence, or the strongest evidence yet, that insulin secretion, intrinsic to the islet cells, is a key mechanism underlying the associations at the HNF1A, IGF2BP2, KCNQ1, HNF1B, VPS13C/C2CD4A, FAF1, PTPRD, AP3S2, KCNK16, MAEA, LPP, WFS1, and TMPRSS6 loci. The fasting glucose-raising allele near PDX1, a known key insulin transcription factor, was strongly associated with lower first-phase insulin secretion but has no evidence for an effect on type 2 diabetes risk. The diabetes risk allele at TCF7L2 was associated with a stronger effect on peak insulin response than on C-peptide-based insulin secretion rate, suggesting a possible additional role in hepatic insulin clearance or insulin processing. In summary, our study provides further insight into the mechanisms by which common genetic variation influences type 2 diabetes risk and glycemic traits. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng |
653 | a beta-cell function | |
653 | a glycemic traits | |
653 | a transcription-factor-7-like-2 | |
653 | a tcf7l2 | |
653 | a genetic architecture | |
653 | a mexican-americans | |
653 | a proinsulin levels | |
653 | a common variants | |
653 | a iras family | |
653 | a glucose | |
653 | a polymorphisms | |
653 | a lonsky ks | |
653 | a 1988 | |
653 | a journal of clinical investigation | |
653 | a v81 | |
653 | a p435 | |
700 | 1 | a Jonsson, A.4 aut |
700 | 1 | a Jackson, A. U.4 aut |
700 | 1 | a Wang, N.4 aut |
700 | 1 | a van Leewen, N.4 aut |
700 | 1 | a Palmer, N. D.4 aut |
700 | 1 | a Kobes, S.4 aut |
700 | 1 | a Deelen, J.4 aut |
700 | 1 | a Boquete-Vilarino, L.4 aut |
700 | 1 | a Paananen, J.4 aut |
700 | 1 | a Stancakova, A.4 aut |
700 | 1 | a Boomsma, D. I.4 aut |
700 | 1 | a de Geus, E. J. C.4 aut |
700 | 1 | a Eekhoff, E. M. W.4 aut |
700 | 1 | a Fritsche, A.4 aut |
700 | 1 | a Kramer, M.4 aut |
700 | 1 | a Nijpels, G.4 aut |
700 | 1 | a Simonis-Bik, A.4 aut |
700 | 1 | a van Haeften, T. W.4 aut |
700 | 1 | a Mahajan, A.4 aut |
700 | 1 | a Boehnke, M.4 aut |
700 | 1 | a Bergman, R. N.4 aut |
700 | 1 | a Tuomilehto, J.4 aut |
700 | 1 | a Collins, F. S.4 aut |
700 | 1 | a Mohlke, K. L.4 aut |
700 | 1 | a Banasik, K.4 aut |
700 | 1 | a Groves, C. J.4 aut |
700 | 1 | a McCarthy, M. I.4 aut |
700 | 1 | a Pearson, E. R.4 aut |
700 | 1 | a Natali, A.4 aut |
700 | 1 | a Mari, A.4 aut |
700 | 1 | a Buchanan, T. A.4 aut |
700 | 1 | a Taylor, K. D.4 aut |
700 | 1 | a Xiang, A. H.4 aut |
700 | 1 | a Gjesing, A. P.4 aut |
700 | 1 | a Grarup, N.4 aut |
700 | 1 | a Eiberg, H.4 aut |
700 | 1 | a Pedersen, O.4 aut |
700 | 1 | a Chen, Y. D.4 aut |
700 | 1 | a Laakso, M.4 aut |
700 | 1 | a Norris, J. M.4 aut |
700 | 1 | a Smith, Ulf,d 1943u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xsmiul |
700 | 1 | a Wagenknecht, L. E.4 aut |
700 | 1 | a Baier, L.4 aut |
700 | 1 | a Bowden, D. W.4 aut |
700 | 1 | a Hansen, T.4 aut |
700 | 1 | a Walker, M.4 aut |
700 | 1 | a Watanabe, R. M.4 aut |
700 | 1 | a t Hart, L. M.4 aut |
700 | 1 | a Hanson, R. L.4 aut |
700 | 1 | a Frayling, T. M.4 aut |
710 | 2 | a Göteborgs universitetb Institutionen för medicin, avdelningen för molekylär och klinisk medicin4 org |
773 | 0 | t Diabetesd : American Diabetes Associationg 66:8, s. 2296-2309q 66:8<2296-2309x 0012-1797x 1939-327X |
856 | 4 | u https://diabetes.diabetesjournals.org/content/diabetes/66/8/2296.full.pdf |
856 | 4 8 | u https://gup.ub.gu.se/publication/255727 |
856 | 4 8 | u https://doi.org/10.2337/db16-1452 |
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