We conducted a two-stage association study in individuals of European descent (Online Methods, Supplementary Figure 1, Supplementary Tables 1a and b). Because we sought to identify variants that influence FG in the normal population, hyperglycemia in the diabetic range exerts deleterious effects on β-cell function20,21, and treatment can confound glucose and insulin measurements, we excluded individuals with known diabetes, on anti-diabetic treatment, or with FG ≥7 mmol/L. We combined data from 21 Stage 1 discovery GWAS for FG (N=46,186) and 20 GWAS for FI (N=38,238), HOMA-B (N=36,466) and HOMA-IR (N=37,037), and analyzed associations for ~2.5M autosomal SNPs directly genotyped and imputed22,23 from HapMap CEU sample data assuming an additive genetic effect for each of the four traits.