Effect of streptozotocin-induced diabetes mellitus on release of vasoactive intestinal polypeptide from rodent small intestine.

Representative longitudinal muscle strips (6 x 10 mm) from proximal and distal small intestine were excised from control and streptozotocin-treated rats after one month of untreated and insulin-treated diabetes. Untreated diabetes significantly reduced tissue concentrations of vasoactive intestinal polypeptide (VIP) at both intestinal loci. Insulin treatment of the diabetic animals restored tissue VIP concentrations to control group levels, although the beneficial effect of insulin treatment was only significant in the duodenum. Spontaneous release of VIP was significantly attenuated by untreated diabetes at both intestinal sites. In the duodenum, insulin treatment of the diabetic animals restored VIP release to levels indistinguishable from control group values. In the ileum, insulin treatment produced levels of VIP release that were not significantly different from those of the control and untreated diabetic groups. Tetrodotoxin (5 x 10(-6) M) significantly--but incompletely--inhibited VIP release from control group animals at both intestinal sites. These observations indicate that diabetes mellitus significantly diminishes VIP tissue concentrations and release from intestinal myenteric nerves. These abnormalities improve with insulin treatment. However, the mechanisms of VIP release from proximal and distal intestine appear to differ not only in their response to the diabetic state, but also in their response to insulin treatment.

[Ulcer disease of endocrine origin associated with a non-gastrin substance]. / Maladie ulcéreuse d'origine endocrine véhiculée par une substance non-gastrinique.

The purpose of this paper is to report on a form of duodenal ulceration associated with a major hypersecretion that we described in 1984. This entity belongs to the group of endocrine duodenal ulcer diatheses of which the Zollinger-Ellison Syndrome (ZES) in the prototype. We have recently in 1989 reported a series of patients with clinical and pathologic features indistinguishable from those of the Zollinger-Ellison syndrome but without hypergastrinemia. We have also found that the plasma and the tumor tissues of these patients contains a potent non-gastrin secretagogue.