The rate of gastric emptying is controlled by humoral and nerval factors. When glucose, fat, or amino come into contact with the duodenal mucosa inhibitory mechanisms decrease the fundic pressure and thereby slow the gastric emptying of nutrients. Among the various peptides, so far investigated, gastrin inhibits the emptying rate, however, this effect is only seen at unphysiological high concentrations. Cholecystokinin, on the other hand, is able to decrease the delivery of glucose to the duodenum at physiological concentrations. Also secretin exerts an inhibitory effect on gastric emptying. The peptide YY which is released from the ileum and colon after ingestion of carbohydrates or fat and which inhibits gastric acid secretion also reduces the amount of food emptied from the stomach. This inhibitory effect was achieved by doses which are within the physiological range. The neuropeptide vasoactive intestinal polypeptide (VIP) and the enkephalins are both able to retard the gastric emptying. Some of these effects, especially of VIP, are mediated by noncholinergic, non-adrenergic inhibitory vagal nerves. Stimulation of gastric emptying is seen with motilin and somatostatin. The effect of motilin is a direct one, whereas the effect of somatostatin is probably due to inhibition of regulatory peptides which in turn inhibit the emptying in the sense of a feedback. So far, these peptides which are responsible for the inhibitory effect of gastric emptying following the presence of carbohydrates in the duodenum, have not yet been elucidated. The rate of glucose delivery to the duodenum determines the shape of the blood glucose curve and either directly via the blood glucose or indirectly via the release of insulinotropic gut hormones, also the amount of insulin secreted.