Literature DB >> 19557384

IRS1 G972R polymorphism and type 2 diabetes: a paradigm for the difficult ascertainment of the contribution to disease susceptibility of 'low-frequency-low-risk' variants.

E Morini1, S Prudente, E Succurro, M Chandalia, Y-Y Zhang, S Mammarella, F Pellegrini, C Powers, V Proto, B Dallapiccola, A Cama, G Sesti, N Abate, A Doria, V Trischitta.   

Abstract

AIMS/HYPOTHESIS: The aim of the study was to determine the association between IRS1 G972R polymorphism and type 2 diabetes; published data concerning this association have been conflicting. To obtain further insight into this topic, we performed a meta-analysis of all available case-control studies.
METHODS: We performed a meta-analysis of 32 studies (12,076 cases and 11,285 controls).
RESULTS: The relatively infrequent R972 variant was not significantly associated with type 2 diabetes (OR 1.09, 95% CI 0.96-1.23, p = 0.184 under a dominant model). Some evidence of heterogeneity was observed across studies (p = 0.1). In the 14 studies (9,713 individuals) in which the mean age at type 2 diabetes diagnosis was available, this variable explained 52% of the heterogeneity (p = 0.03). When these studies were subdivided into tertiles of mean age at diagnosis, the OR for diabetes was 1.48 (95% CI 1.17-1.87), 1.22 (95% CI 0.97-1.53) and 0.88 (95% CI 0.68-1.13) in the youngest, intermediate and oldest tertile, respectively (p = 0.0022 for trend of ORs). CONCLUSIONS/
INTERPRETATION: Our findings illustrate the difficulties of ascertaining the contribution of 'low-frequency-low-risk' variants to type 2 diabetes susceptibility. In the specific context of the R972 variant, approximately 200,000 study individuals would be needed to have 80% power to identify a 9% increase in diabetes risk at a genome-wide significance level. Under these circumstances, a strategy aimed at improving outcome definition and decreasing its heterogeneity may critically enhance our ability to detect genetic effects, thereby decreasing the required sample size. Our data suggest that focusing on early-onset diabetes, which is characterised by a stronger genetic background, may be part of such a strategy.

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Year:  2009        PMID: 19557384      PMCID: PMC2782547          DOI: 10.1007/s00125-009-1426-4

Source DB:  PubMed          Journal:  Diabetologia        ISSN: 0012-186X            Impact factor:   10.122


  18 in total

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4.  Insulin secretory function is impaired in isolated human islets carrying the Gly(972)-->Arg IRS-1 polymorphism.

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5.  The Gly972Arg polymorphism in the insulin receptor substrate-1 gene contributes to the variation in insulin secretion in normal glucose-tolerant humans.

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6.  The TRIB3 Q84R polymorphism and risk of early-onset type 2 diabetes.

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Review 8.  Defects of the insulin receptor substrate (IRS) system in human metabolic disorders.

Authors:  G Sesti; M Federici; M L Hribal; D Lauro; P Sbraccia; R Lauro
Journal:  FASEB J       Date:  2001-10       Impact factor: 5.191

9.  Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes.

Authors:  Eleftheria Zeggini; Laura J Scott; Richa Saxena; Benjamin F Voight; Jonathan L Marchini; Tianle Hu; Paul I W de Bakker; Gonçalo R Abecasis; Peter Almgren; Gitte Andersen; Kristin Ardlie; Kristina Bengtsson Boström; Richard N Bergman; Lori L Bonnycastle; Knut Borch-Johnsen; Noël P Burtt; Hong Chen; Peter S Chines; Mark J Daly; Parimal Deodhar; Chia-Jen Ding; Alex S F Doney; William L Duren; Katherine S Elliott; Michael R Erdos; Timothy M Frayling; Rachel M Freathy; Lauren Gianniny; Harald Grallert; Niels Grarup; Christopher J Groves; Candace Guiducci; Torben Hansen; Christian Herder; Graham A Hitman; Thomas E Hughes; Bo Isomaa; Anne U Jackson; Torben Jørgensen; Augustine Kong; Kari Kubalanza; Finny G Kuruvilla; Johanna Kuusisto; Claudia Langenberg; Hana Lango; Torsten Lauritzen; Yun Li; Cecilia M Lindgren; Valeriya Lyssenko; Amanda F Marvelle; Christa Meisinger; Kristian Midthjell; Karen L Mohlke; Mario A Morken; Andrew D Morris; Narisu Narisu; Peter Nilsson; Katharine R Owen; Colin N A Palmer; Felicity Payne; John R B Perry; Elin Pettersen; Carl Platou; Inga Prokopenko; Lu Qi; Li Qin; Nigel W Rayner; Matthew Rees; Jeffrey J Roix; Anelli Sandbaek; Beverley Shields; Marketa Sjögren; Valgerdur Steinthorsdottir; Heather M Stringham; Amy J Swift; Gudmar Thorleifsson; Unnur Thorsteinsdottir; Nicholas J Timpson; Tiinamaija Tuomi; Jaakko Tuomilehto; Mark Walker; Richard M Watanabe; Michael N Weedon; Cristen J Willer; Thomas Illig; Kristian Hveem; Frank B Hu; Markku Laakso; Kari Stefansson; Oluf Pedersen; Nicholas J Wareham; Inês Barroso; Andrew T Hattersley; Francis S Collins; Leif Groop; Mark I McCarthy; Michael Boehnke; David Altshuler
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Review 4.  Insulin signaling regulating genes: effect on T2DM and cardiovascular risk.

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5.  Insulin receptor substrate 1 (IRS1) variants confer risk of diabetes in the Boston Puerto Rican Health Study.

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6.  Current Insights into the Joint Genetic Basis of Type 2 Diabetes and Coronary Heart Disease.

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8.  Association study of a common variant near IRS1 with type 2 diabetes mellitus in Chinese Han population.

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10.  IRS1 gene variants, dysglycaemic metabolic changes and type-2 diabetes risk.

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