Previous studies showed that tissue expression and actions of URAT1 in the kidney and adipose tissues are enhanced in an insulin-resistant state, presumably via persistent exposure to hyperinsulinemia, hyperuricemia, and hypercholesterolemia, including high PA (namely, the factors all of which are deeply involved in the pathophysiology of metabolic syndrome and could develop the current model of metabolic heart disease).7 Here, INS is linked to metabolic syndrome.