STIMULATION OF GLYCOGENOLYSIS BY 3 LOCUST ADIPOKINETIC HORMONES INVOLVES G(S) AND CAMP

Insect adipokinetic hormones (AKHs) have been shown to mobilize fat bo dy carbohydrate by glycogen phosphorylase activation. In this study, t he signal transduction pathways of AKH-I, -II and -III from the migrat ory locust are further elucidated. We show that the AKHs enhance fat b ody cAMP levels in vitro. For all hormones, maximal levels are reached after 1 min and correspond to a 200% increase compared to resting lev els. Although cAMP levels induced by massive doses of AKH-I, -II and - III are equal, AKH-III is the most potent when applied in a physiologi cal dose. This difference in potency also applies to glycogen phosphor ylase activation. Cholera toxin (CTX) likewise enhances cAMP levels an d phosphorylase activity, however pertussis toxin (PTX) has no effect. Increases induced by CTX and AKH are not additive, suggesting that th ey share the same pathway. Phosphorylase activation by the AKHs is str ongly attenuated by guanosine-5'-O-(2-thiodiphosphate) (GDP beta S). T hese results demonstrate a role for cAMP in AKH signal transduction an d indicate that the AKH receptor(s) are coupled to cAMP formation and glycogen phosphorylase activation via the stimulatory guanine nucleoti de-binding protein (G(s)).