In addition to insulin resistance, enhanced response of insulin counter-regulatory hormones such as glucagon and its Drosophila homolog, adipokinetic hormone (Akh), has been shown to cause high-caloric diet-induced hyperglycemia across species. Many groups including ours have previously characterized regulatory components transducing linear Akh signaling that promotes carbohydrate production through glycogenolysis and gluconeogenesis. The spatial elucidation of Akh action at the organelle levels, however, still remains largely unknown. In this study, we revealed that Akh phosphorylates ERK and translocates it to peroxisome, mediates fat body peroxisomal conversion of amino acids from circulation into carbohydrate for subsequent gluconeogenesis in response to Akh.