If mitochondrial dysfunction is, indeed, the underlying cellular defect that explains abnormal glucose metabolism, agents that enhance mitochondrial function—such as uridine— may improve glucose homeostasis in this and other insulin-resistant states (e.g. type 2 diabetes, the metabolic syndrome, polycystic ovary syndrome, and nonalcoholic steatohepatitis). The gene discussed is INS; the disease is type 2 diabetes mellitus.