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01.12.2012 | Review | Ausgabe 1/2012 Open Access

Cardiovascular Diabetology 1/2012

Identification of shared genetic susceptibility locus for coronary artery disease, type 2 diabetes and obesity: a meta-analysis of genome-wide studies

Zeitschrift:
Cardiovascular Diabetology > Ausgabe 1/2012
Autoren:
Chaoneng Wu, Yunguo Gong, Jie Yuan, Hui Gong, Yunzeng Zou, Junbo Ge
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2840-11-68) contains supplementary material, which is available to authorized users.
Chaoneng Wu, Yunguo Gong contributed equally to this work.

Competing interests

The authors declare that they have no conflicts of interest.

Authors’ contributions

Chaoneng Wu and Yunguo Gong participated in designing, carried out the literature reviewing and data stastical analysis, and drafting the manuscript. Jie Yuan and Hui Gong participated in literature reviewing and data extraction. Yunzeng Zou and Junbo Ge conceived of the study, and participated in its design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.

Abstract

Type 2 diabetes (2DM), obesity, and coronary artery disease (CAD) are frequently coexisted being as key components of metabolic syndrome. Whether there is shared genetic background underlying these diseases remained unclear. We performed a meta-analysis of 35 genome screens for 2DM, 36 for obesity or body mass index (BMI)-defined obesity, and 21 for CAD using genome search meta-analysis (GSMA), which combines linkage results to identify regions with only weak evidence and provide genetic interactions among different diseases. For each study, 120 genomic bins of approximately 30 cM were defined and ranked according to the best linkage evidence within each bin. For each disease, bin 6.2 achieved genomic significanct evidence, and bin 9.3, 10.5, 16.3 reached suggestive level for 2DM. Bin 11.2 and 16.3, and bin 10.5 and 9.3, reached suggestive evidence for obesity and CAD respectively. In pooled all three diseases, bin 9.3 and 6.5 reached genomic significant and suggestive evidence respectively, being relatively much weaker for 2DM/CAD or 2DM/obesity or CAD/obesity. Further, genomewide significant evidence was observed of bin 16.3 and 4.5 for 2DM/obesity, which is decreased when CAD was added. These findings indicated that bin 9.3 and 6.5 are most likely to be shared by 2DM, obesity and CAD. And bin 16.3 and 4.5 are potentially common regions to 2DM and obesity only. The observed shared susceptibility regions imply a partly overlapping genetic aspects of disease development. Fine scanning of these regions will definitely identify more susceptibility genes and causal variants.
Zusatzmaterial
Additional file 1: Table S1. Characteristics of whole genome studies of T2D [42–75,2]. Table S2. Characteristics of whole genome studies of obesity or BMI-defined obesity [76–111]. Table S3. Characteristics of whole genome studies of CAD [112–132]. (DOC 245 KB)
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Authors’ original file for figure 1
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Authors’ original file for figure 2
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