The accumulation of central adiposity has serious adverse health consequences including hyperlipidemia and increased risks of T2D. We examined the relationships between adiposity-related SNPs and these clinical phenotypes using available GWAS meta-analysis data (Text S1). We found an association between the WHR-increasing G-allele of rs2605100 (LYPLAL1) and increased fasting triglycerides (P = 3.9×10−4; Table S8) in data from a recent GWAS meta-analysis of 14,343 European samples [28]. This is further supported by a parallel GWAS meta-analysis effort in 19,840 samples where the G allele is similarly associated with increased triglycerides (P = 0.02) [29]. Using T2D case-control data from the DIAGRAM consortium [30], we found directionally-consistent, though only weak, associations with T2D-risk, most obviously at TFAP2B (P = 0.09; Table S9). An association between other non-HapMap TFAP2B variants and T2D has previously been reported in Japanese samples [21]. These T2D-associated variants show modest linkage disequilibrium to our WC associated SNP in UK samples (IVS1774_G/T and rs987237, r2 = 0.42; intron_1+2093_(A/C) and rs987237, r2 = 0.67). Thus, we see some evidence that the variants identified have anticipated effects on downstream phenotypes,
