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Insulin resistance (IR) is a key determinant of type 2 diabetes (T2D) and other metabolic disorders. This genome-wide association study (GWAS) was designed to shed light on the genetic basis of fasting insulin (FI) and IR in 927 non-diabetic African Americans. 5 396 838 single-nucleotide polymorphisms (SNPs) were tested for associations with FI or IR with adjustments for age, sex, body mass index, hypertension status and first two principal components. Genotyped SNPs ( n  = 12) with  P  &lt; 5 × 10 −6  in African Americans were carried forward for  de novo  genotyping in 570 non-diabetic West Africans. We replicated SNPs in or near  SC4MOL  and  TCERG1L  in West Africans. The meta-analysis of 1497 African Americans and West Africans yielded genome-wide significant associations for SNPs in the  SC4MOL  gene: rs17046216 ( P  = 1.7 × 10 −8  and 2.9 × 10 −8  for FI and IR, respectively); and near the  TCERG1L  gene with rs7077836 as the top scoring ( P  = 7.5 × 10 −9  and 4.9 × 10 −10  for FI and IR, respectively).  In silico  replication in the MAGIC study ( n  = 37 037) showed weak but significant association (adjusted  P -value of 0.0097) for rs34602777 in the  MYO5A  gene. In addition, we replicated previous GWAS findings for IR and FI in Europeans for  GCKR , and for variants in four T2D loci ( FTO ,  IRS1 ,  KLF14  and  PPARG ) which exert their action via IR. In summary, variants in/near  SC4MOL , and  TCERG1L  were associated with FI and IR in this cohort of African Americans and were replicated in West Africans.  SC4MOL  is under-expressed in an animal model of T2D and plays a key role in lipid biosynthesis, with implications for the regulation of energy metabolism, obesity and dyslipidemia.  TCERG1L  is associated with plasma adiponectin, a key modulator of obesity, inflammation, IR and diabetes.

Genome-wide association study identifies novel loci association with fasting insulin and insulin resistance in African Americans