A mechanistic explanation of the link of Cu-D5D-T2D is that lower Cu increases hepatic SREBP-1 activation [48], which transcriptionally upregulates FADS1 (D5D) expression [49], favoring the conversion of 20:3n-6 to 20:4n-6 and thereby reducing circulating 20:3n-6 levels, which are associated with increased T2D risk [3]. This evidence concerns the gene FADS1 and type 2 diabetes mellitus.