The description of the incretin effect was first described in 1964 by Elwick when he observed a greater insulin secretory response if glucose was administered orally compared to intravenously despite similar elevations in plasma glucose. This incretin effect is attributed to the release of peptide hormones from the K and L cells in the intestines in the response to eating, so that approximately 60% of the insulin subsequently secreted is related directly to the effect of incretins [1]. Glucagon like peptide-1 (GLP-1) is secreted by the L cells, suppresses postprandial glucagon secretion, reduces appetite and stimulates insulin secretion in a dose dependent manner.