In this study, catalpol reduced blood glucose, ameliorated hepatic insulin resistance and reduced diabetes-associated hepatic injury and steatosis [53]; as well as activation of AMPK, catalpol treatment was associated with increased GSK3β phosphorylation, reduced glycogen synthase phosphorylation, stimulation of hepatic glycogen synthesis and inhibition of hepatic gluconeogenesis. Here, PRKAA1 is linked to Insulin resistance.