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Insulin release from the beta cells is influenced by nutrients (both carbohydrates and non-carbohydrates), hormonal factors including gut hormones and neural factors. Of all these insulin secretagogues, glucose availability is the major physiological determinant of insulin secretion. The insulin secretory response is greater after oral administration of glucose than after intravenous glucose administration (Fig – 1), an indication that absorption of glucose by way of gastro-intestinal tract stimulates the release of hormones and other mechanism that ultimately enhance the sensitivity of the beta cell to glucose. This phenomenon is known as ‘Incretin effect ’ and is facilitated by gut hormones. Glucagon is secreted from α cells and functions predominantly during the fasting state to maintain blood glucose levels by the mobilization of glucose from glycogen stores in peripheral tissues such as muscle and liver. Excessive production of glucagon contributes to hyperglycemia and thus approaches that antagonize glucagon action in subjects with diabetes are being actively investigated. Two aspects of the gut have interested the diabetologists over the past 30 years. They are the incretin effect and the occurrence of glucagon-producing L-cells in the gut. The incretin effect is the amplification of nutrient-induced insulin secretion by hormones from the gut particularly GIP (gastric inhibitory peptide) and GLP 1 (glucagon like peptide 1)1 [Fig – 2]. Of these two peptides, GLP 1 is the most potent and efficacious insulinotrophic hormone1. Th