Effects of somatostatin on the exocrine pancreas and the release of duodenal hormones

Abstract Using "the artificial beta cell," previous studies have demonstrated that in insulin-dependent diabetics somatostatin reduces insulin requirements up to 70% and causes a marked flattening of the blood glucose curve after food intake. 1 Furthermore, in insulin-dependent diabetics somatostatin diminishes by 75%–100% rises in blood glucose after oral glucose, but did not influence glucose levels following intravenous glucose. 2 Since during the somatostatin infusion, a 30% reduction in splanchnic blood flow was observed, 2 the diminution of postprandial hypoglycemia following somatostatin seemed attributable primarily to a circulation-dependent delay in carbohydrate absorption. The fact that radioimmunoassayable somatostatin has been found not only in the stomach of the rat but also in the upper intestine, 3 in amounts comparable to those found in the hypothalamus, allow the assumption that somatostatin is a hormone in the gastrointestinal tract, coordinating the secretion of the other hormones. Recently, somatostatin-positive cells were shown to be present in the bottom of the intestinal crypt by immunohistochemical methods; 18 these cells were distinguished from those in other organs by the presence of a cytoplasmic process reaching the gut lumen (external environment). The assumed physiological importance of somatostatin or a somatostatin-like substance in the alimentary tract is emphasized by the fact that recently 4 a somatostatin-like immunoreactive peptide was isolated from the porcine duodenum. It has been known for many years that various gastrointestinal hormones exert an influence on the blood flow of the gastrointestinal tract. 5,6 It is unclear whether the effect of somatostatin on the splanchnic blood flow can be explained by the inhibition of various gastrointestinal hormones. The fact that in insulin-dependent diabetics somatostatin did not improve the intravenous glucose tolerance but only the peroral one suggests that the different effects of somatostatin in the gut may be partly the result of inhibition of various duodenal hormones. The present studies were undertaken to characterize the influence of somatostatin on the release and the biological activities of the two classic intestinal hormones, secretin and pancreozymin.