Administration of GLP-1 or one of its mimetics has been shown to promote the preservation or expansion of β-cell mass and to delay the development of diabetes in animal models, although not yet in human subjects. This effect may be partly the result of improved glycaemic control. However, elevated intracellular cAMP levels have been shown to protect β-cells from 2-deoxy-d-ribose-induced oxidative damage and lipid-induced apoptosis. As GPR119 agonists raise cAMP levels in the β-cell, there is potential for these agents to exert a beneficial effect on disease progression beyond what could be achieved by improving glucose homoeostasis alone. The concomitant increase in circulating GLP-1, itself capable of raising β-cell cAMP levels, might contribute to such an effect.