PLoS Genetics (May 2012)
Stratifying type 2 diabetes cases by BMI identifies genetic risk variants in LAMA1 and enrichment for risk variants in lean compared to obese cases.
- John R B Perry,
- Benjamin F Voight,
- Loïc Yengo,
- Najaf Amin,
- Josée Dupuis,
- Martha Ganser,
- Harald Grallert,
- Pau Navarro,
- Man Li,
- Lu Qi,
- Valgerdur Steinthorsdottir,
- Robert A Scott,
- Peter Almgren,
- Dan E Arking,
- Yurii Aulchenko,
- Beverley Balkau,
- Rafn Benediktsson,
- Richard N Bergman,
- Eric Boerwinkle,
- Lori Bonnycastle,
- Noël P Burtt,
- Harry Campbell,
- Guillaume Charpentier,
- Francis S Collins,
- Christian Gieger,
- Todd Green,
- Samy Hadjadj,
- Andrew T Hattersley,
- Christian Herder,
- Albert Hofman,
- Andrew D Johnson,
- Anna Kottgen,
- Peter Kraft,
- Yann Labrune,
- Claudia Langenberg,
- Alisa K Manning,
- Karen L Mohlke,
- Andrew P Morris,
- Ben Oostra,
- James Pankow,
- Ann-Kristin Petersen,
- Peter P Pramstaller,
- Inga Prokopenko,
- Wolfgang Rathmann,
- William Rayner,
- Michael Roden,
- Igor Rudan,
- Denis Rybin,
- Laura J Scott,
- Gunnar Sigurdsson,
- Rob Sladek,
- Gudmar Thorleifsson,
- Unnur Thorsteinsdottir,
- Jaakko Tuomilehto,
- Andre G Uitterlinden,
- Sidonie Vivequin,
- Michael N Weedon,
- Alan F Wright,
- MAGIC,
- DIAGRAM Consortium,
- GIANT Consortium,
- Frank B Hu,
- Thomas Illig,
- Linda Kao,
- James B Meigs,
- James F Wilson,
- Kari Stefansson,
- Cornelia van Duijn,
- David Altschuler,
- Andrew D Morris,
- Michael Boehnke,
- Mark I McCarthy,
- Philippe Froguel,
- Colin N A Palmer,
- Nicholas J Wareham,
- Leif Groop,
- Timothy M Frayling,
- Stéphane Cauchi
Affiliations
- John R B Perry
- Benjamin F Voight
- Loïc Yengo
- Najaf Amin
- Josée Dupuis
- Martha Ganser
- Harald Grallert
- Pau Navarro
- Man Li
- Lu Qi
- Valgerdur Steinthorsdottir
- Robert A Scott
- Peter Almgren
- Dan E Arking
- Yurii Aulchenko
- Beverley Balkau
- Rafn Benediktsson
- Richard N Bergman
- Eric Boerwinkle
- Lori Bonnycastle
- Noël P Burtt
- Harry Campbell
- Guillaume Charpentier
- Francis S Collins
- Christian Gieger
- Todd Green
- Samy Hadjadj
- Andrew T Hattersley
- Christian Herder
- Albert Hofman
- Andrew D Johnson
- Anna Kottgen
- Peter Kraft
- Yann Labrune
- Claudia Langenberg
- Alisa K Manning
- Karen L Mohlke
- Andrew P Morris
- Ben Oostra
- James Pankow
- Ann-Kristin Petersen
- Peter P Pramstaller
- Inga Prokopenko
- Wolfgang Rathmann
- William Rayner
- Michael Roden
- Igor Rudan
- Denis Rybin
- Laura J Scott
- Gunnar Sigurdsson
- Rob Sladek
- Gudmar Thorleifsson
- Unnur Thorsteinsdottir
- Jaakko Tuomilehto
- Andre G Uitterlinden
- Sidonie Vivequin
- Michael N Weedon
- Alan F Wright
- MAGIC
- DIAGRAM Consortium
- GIANT Consortium
- Frank B Hu
- Thomas Illig
- Linda Kao
- James B Meigs
- James F Wilson
- Kari Stefansson
- Cornelia van Duijn
- David Altschuler
- Andrew D Morris
- Michael Boehnke
- Mark I McCarthy
- Philippe Froguel
- Colin N A Palmer
- Nicholas J Wareham
- Leif Groop
- Timothy M Frayling
- Stéphane Cauchi
- DOI
- https://doi.org/10.1371/journal.pgen.1002741
- Journal volume & issue
-
Vol. 8,
no. 5
p. e1002741
Abstract
Common diseases such as type 2 diabetes are phenotypically heterogeneous. Obesity is a major risk factor for type 2 diabetes, but patients vary appreciably in body mass index. We hypothesized that the genetic predisposition to the disease may be different in lean (BMI<25 Kg/m²) compared to obese cases (BMI≥30 Kg/m²). We performed two case-control genome-wide studies using two accepted cut-offs for defining individuals as overweight or obese. We used 2,112 lean type 2 diabetes cases (BMI<25 kg/m²) or 4,123 obese cases (BMI≥30 kg/m²), and 54,412 un-stratified controls. Replication was performed in 2,881 lean cases or 8,702 obese cases, and 18,957 un-stratified controls. To assess the effects of known signals, we tested the individual and combined effects of SNPs representing 36 type 2 diabetes loci. After combining data from discovery and replication datasets, we identified two signals not previously reported in Europeans. A variant (rs8090011) in the LAMA1 gene was associated with type 2 diabetes in lean cases (P = 8.4×10⁻⁹, OR = 1.13 [95% CI 1.09-1.18]), and this association was stronger than that in obese cases (P = 0.04, OR = 1.03 [95% CI 1.00-1.06]). A variant in HMG20A--previously identified in South Asians but not Europeans--was associated with type 2 diabetes in obese cases (P = 1.3×10⁻⁸, OR = 1.11 [95% CI 1.07-1.15]), although this association was not significantly stronger than that in lean cases (P = 0.02, OR = 1.09 [95% CI 1.02-1.17]). For 36 known type 2 diabetes loci, 29 had a larger odds ratio in the lean compared to obese (binomial P = 0.0002). In the lean analysis, we observed a weighted per-risk allele OR = 1.13 [95% CI 1.10-1.17], P = 3.2×10⁻¹⁴. This was larger than the same model fitted in the obese analysis where the OR = 1.06 [95% CI 1.05-1.08], P = 2.2×10⁻¹⁶. This study provides evidence that stratification of type 2 diabetes cases by BMI may help identify additional risk variants and that lean cases may have a stronger genetic predisposition to type 2 diabetes.