The effect of glycosyl inositol-phosphate on cAMP production in isolated rat fat-cells is transduced by a pertussis toxin sensitive G-protein.

In fat-cells, insulin increases synergistically the inhibitory effects of adenosine and prostaglandin E2 on adenylyl cyclase activity. When the endogenous production of these feedback inhibitors is suppressed, insulin is no more active in conditions where glycosyl inositol-phosphate which is a putative mediator of its action, is always efficient. Moreover, glycosyl inositol-phosphate signal is transduced by a G protein sensitive to IAP intoxication.