Published studies utilizing 12-LOX knockout mouse models and pharmacologic inhibition of 12-LOX reported protective outcomes that resulted from inactivation of 12-LOX, which include improved glucose tolerance and insulin sensitivity following HF feeding, resistance to the development of diabetes by increasing islet resistance to inflammatory cytokines such as tumor necrosis factor α and IL-1β, and reduction of infarct size in ischemic damage (14, 33, 34, 35, 36, 37). This evidence concerns the gene ALOX12 and diabetes mellitus.