Genome wide association study identifies KCNMA1contributing to human obesity

BMC Medical Genomics

Table 1 Cohorts for genetic studies

				obese cases			lean and population-based controls
	Cohort	SNP§	Nationality	female/male	BMI* (kg/m²)	age* (years)	female/male	BMI* (kg/m²)	age* (years)
Discovery	1	406,177	Swedish	131/33^§	44.7 ± 4.7	43.8 ± 12.6	137/26	22.2 ± 1.8	51.6 ± 6.1
Replication	2	700	Swedish	370/90^§§	44.6 ± 4.6	42.2 ± 13.2	206/41	22.6 ± 1.7	51.6 ± 5.3
Replication	3	21	Swedish	1025/789	37.1 ± 5.4	46.6 ± 11.4	819/885	22.8 ± 1.7	48.7 ± 10.8
Replication	4**	21	French	641/344	33.7 ± 8.2	14.1 ± 5.0	289/243^#	18.7 ± 3.3	11.8 ± 1.6
Replication	5	2	French	682/246	48.5 ± 7.6	43.0 ± 12.1	1630/1108^#	23.8 ± 3.5	49.7 ± 6.3
Replication	6**	2	German	278/209	33.4 ± 6.8	14.4 ± 3.7	271/171	18.3 ± 1.1	16.1 ± 5.8
Total				3127/1711			3353/2474

* Values are mean ± SD; ** Cohorts comprising children in which case BMI Z-scores were used to define obesity status as defined in Methods.
§ Number of SNPs genotyped in each cohort. The 700 most significantly obesity associated SNPs in the GWA were analyzed in cohort 2 (threshold P = 0.003). Subsequently, nominal association with obesity was used as threshold to determine whether a SNP would be followed up by genotyping additional cohorts. # population-based controls

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