INS and hyperuricemia: Given that GLUT9a is the sole transporter for basolateral exit of reabsorbed urate into blood (Kimura et al., 2014; Mandal and Mount, 2015) and renal insulin sensitivity remains preserved in hyperinsulinemia (Nizar et al., 2018), we propose that activation of GLUT9a by insulin is a key driver of the renal urate retention in metabolic syndrome associated with hyperuricemia and gout.