As listed in Table 1, candidate gene approach and large-scale high-density genome-wide association studies have identified new loci for common obesity. The discovery of these loci has initiated a series of experiments to explore the pathophysiological mechanisms that underlie obesity development, in particular to the fat mass and obesity-associated (FTO) gene. In 2007, SNPs within the FTO became the first to be associated reproducibly with human body mass. To date, of all identified loci, the genetic variation in FTO has the largest effect on obesity susceptibility [40]. FTO encodes a Fe(II)- and 2-oxoglutarate-dependent oxygenase putatively involved in DNA demethylation. Studies in rodents suggested that FTO mRNA is most abundant in the hypothalamic regions, which control energy homeostasis. The FTO protein shows wide expression patterns in central as well as peripheral regions [41]. Study also demonstrated that increased adipose tissue FTO mRNA was associated with increased BMI in healthy women [41]. FTO -null mice have reduced fat mass, and mice with FTO overexpression displayed increased energy intake and increased adiposity [42, 43]. Despite recent progress, the mechanism by which FTO influences
