Neuroendocrine changes in rat stomach during experimental diabetes mellitus

The effects of 48 days of streptozotocin-induced diabetes mellitus in rats on plasma concentrations of gastrin, somatostatin, pancreatic glucagon, and enteroglucagon have been assessed. In addition, neuroendocrine changes in sections of gastric mucosa were quantified using a computer-assisted morphometric system following immunohistochemical staining with polyclonal antibodies directed against gastrin, PGP 9.5 (a neural protein), and somatostatin. Diabetes resulted in significantly increased fasting plasma concentrations of somatostatin, and entero- and pancreatic glucagon. In contrast, lower plasma gastrin concentrations and decreased antral G-cell density were noted in diabetic rats. Gastric somatostatin and neuronal PGP 9.5 stain densities were unaltered by diabetes. Stomachs of diabetic rats weighed less, but both the jejunum and ileum showed evidence of mucosal hyperplasia. The gastric neuroendocrine atrophy observed in diabetes may be a consequence of elevated plasma somatostatin derived from nongastric sources. The enhanced growth of the intestinal mucosa may be related, directly or indirectly, to raised intraluminal glucose concentration in diabetes.