and minor allele homozygotes at each of the obesity-associated loci, with the weight difference attributable to total, abdominal and gynoid adipose tissue overlaid. While these data illustrate that the weight differences observed for all of the variants are largely related to increased adiposity, for some loci fairly large proportions of the weight difference between homozygotes is attributable to lean mass. For example, the FTO, MCTH2 and TMEM18 variants were predominantly associated with adipose accumulation, whereas the variances in weight for the SH2B1 and NEGR1 variants appear to be explained to a larger extent by the accumulation of non-adipose tissue (e.g. bone, muscle and organ tissue). These characteristics may be of relevance when considering the importance of these variants in cardiovascular and metabolic disease etiology. This is because the health risks associated with weight gain vary depending on whether fat or lean tissue is the source of the accumulated weight.
