Studies in other ethnicities, particularly African-derived populations, are potentially valuable as they may help to fine map the signals of association and, because additional variants present at high frequency in African-derived populations may be absent or rare in European samples.48 Additionally, it is not clear whether associations found in the European samples can be consistently replicated in the samples of predominantly recent African ancestry; genetic, environmental or phenotypic heterogeneity, gene by environment interactions, or different recombination histories between populations could all contribute to a lack of replication in African-derived populations. Along with differences in the prevalence of obesity between African-American and European-derived populations, there are also ethnic differences in metabolic risk factors.49 African Americans have different distribution of fat, with lower amounts of visceral fat, compared with the non-Hispanic whites.50 In summary, we replicated association of seven key SNPs at four loci (NEGR1, TMEM18, SH2B1 and MC4R) in six African-American cohorts that demonstrated consistent association with previous studies of adiposity in Europeans. These loci are all highly expressed in the brain (and several especially in the hypothalamus), consistent with an
