Bariatric surgery mainly includes gastric banding, GB, and Roux-en Y Gastric Bypass, RYGB and both cause weight loss and diabetes (T2DM) resolution. Whereas after GB, diabetes resolution develops gradually in parallel with weight loss and in only about 50% of patients. With T2DM, resolution is almost instantaneous and obtained in 84% after RYGB, prompting a search for associated mechanisms. The abnormal exposure of more distal parts of the small intestine to nutrients and digestive secretions after RYGB suggested that secretion of distal gut hormones could be responsible. Indeed, the secretion of GLP-1 and PYY may be up to 20-fold elevated after RYGB but is unchanged after GB. Both hormones decrease food intake but GLP-1 is strongly insulinotropic. Attempts to block the secretion (somatostatin) or GLP-1 actions (Exendin 9–39) are associated with increased appetite and impaired glucose tolerance. But what causes the exaggerated release. The density of L-cells in the ileum is much higher than in the upper jejunum and this provides part of the explanation. In addition, the passage of nutrients through the bypass and to the ileum may be greatly exaggerated because of bypassing of the upper intestinal mechanisms normally inhibiting gastric emptying (explaining the tendency to dumping after RYGB). Finally, recent studies have revealed expression on the L-cells secreting PYY and GLP-1 of stimulatory receptors for bile acids and lipids to which these cells are now abnormally exposed. Thus, the mechanism is most likely to represent exaggerated activation of the normal "ileal brake" mechanism, with GLP-1 playing a predominant role for the resolution of diabetes.