Genetics
Obesity (2009) 17 7, 1390–1395. doi:10.1038/oby.2008.669
Lack of Association Between a Common Polymorphism Near the INSIG2 Gene and BMI, Myocardial Infarction, and Cardiovascular Risk Factors
Silke Wiedmann1, Katharina Neureuther1, Klaus Stark1, Wibke Reinhard1, Bernd Kallmünzer1, Andrea Baessler1, Marcus Fischer1, Patrick Linsel-Nitschke2, Jeanette Erdmann2, Heribert Schunkert2 and Christian Hengstenberg1
- 1Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany
- 2Medizinische Klinik II, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany
Correspondence: Christian Hengstenberg (christian.hengstenberg@klinik.uni-regensburg.de)
The first two authors contributed equally to this work.
Received 20 June 2008; Accepted 6 October 2008; Published online 5 February 2009.
Abstract
Epidemiological studies revealed an increasing prevalence of and a steep increase in obesity, a risk factor for cardiovascular disease. Because significant influence of a polymorphism, rs7566605, near the INSIG2 gene on BMI has been shown in the general population and in obesity cohorts, we hypothesized that this polymorphism might also act through an elevated BMI on the development of coronary artery disease (CAD) or myocardial infarction (MI). We pursued two strategies: First, the polymorphism rs7566605 was investigated for association with BMI, CAD/MI, and cardiovascular risk factors in a large German cohort at high risk for CAD and MI (n = 1,460 MI patients) as compared to unrelated healthy controls (n = 1,215); second, we extended our analyses on the families of MI patients and performed family-based association testing (n = 5,390 individuals). The polymorphism rs7566605 was analyzed using TaqMan technology. No deviation from Hardy–Weinberg equilibrium could be observed, and the call rate was 98.2%. No significant associations of rs7566605 with CAD/MI, BMI, and classical cardiovascular risk factors could be detected in the full sample size or in the subgroups. A total of 6,878 individuals were investigated in a population of German MI patients and their family members. Although the number of individuals was large enough, no influence of the rs7566605 INSIG2 polymorphism was detected on BMI and CAD/MI. We therefore conclude that in our sample the SNP rs7566605 near the INSIG2 gene does not influence BMI and is not associated directly with CAD/MI or indirectly through cardiovascular risk factors.
