Indeed, previous experiments have shown the physiological importance of hepatic AMPK for glucose homeostasis; liver-specific deletion of AMPKα2 caused hyperglycemia, glucose intolerance, reduced muscle glycogen synthesis, and chronically elevated free fatty acid levels as a result of enhanced gluconeogenesis [41], [42], while short-term over-expression of a constitutively active form of AMPK in the liver results in reduced blood glucose and increased hepatic fatty acid oxidation, suggesting a preference for fatty acid utilization in supplying energy needs [43]. Here, PRKAA1 is linked to Hyperglycemia.