Insulin and cAMP signalling are related to two opposite metabolic responses. Insulin secretion is elicited in response to food availability and trigger catabolic processes like lipogenesis and glycogen synthesis with a purpose of energy storage. On the other hand cAMP signalling is associated with stress and starvation and stimulates processes like glycogen degradation and lipolysis to distribute the stored energy through the body. Although in energy preserving tissues insulin inhibit cAMP signalling, in fat precursor cells cAMP potentiates insulin action and promote adipogenesis. Activation of exchange factor directly activated by cAMP (Epac) has been shown to be crucial for cAMP mediated potentiation of insulin signaling. In the current study I am trying to answer the question as to how cAMP accelerates adipogenesis in vivo as well as what is the role of Epac in cAMP mediated potentiation of insulin signalling. Moreover, I am investigating how increased insulin secretion caused by sucrose consumption, affects insulin signaling in peripheral tissues.