Cholecystokinin, neuropeptide Y and galanin modulate the release of pancreatic somatostatin-25 and somatostatin-14 in vitro.

The direct effects of cholecystokinin (CCK), neuropeptide Y (NPY) and galanin on somatostatin-14 (SS-14) and somatostatin-25 (SS-25), containing [Tyr7, Gly10]-SS-14 at its carboxy terminus and presumably derived from a different gene than that giving rise to SS-14, were evaluated on principal islets (Brockmann bodies) removed from rainbow trout, Oncorhynchus mykiss. The potential for peptidergic action was deduced from the extensive neural network innervating the Brockmann body and confirmed by immunohistochemistry. Immunopositive CCK-like staining was located around the periphery of principal islets as well as in centrally-located nerve tracts. Mammalian CCK-33 stimulated SS-25 release at a dose of 10(-11) M in the presence of 1, 3 and 10 mM glucose. CCK-33 inhibited the release of SS-14 at concentrations of 10(-11) and 10(-7) M only in the presence of high (10 mM) glucose. Mammalian NPY stimulated SS-25 release in a dose-related manner in the presence of low (1 mM) glucose; the efficacy of this effect decreased at higher glucose concentrations. SS-14 release was inhibited by NPY in the presence of 10 mM glucose. Mammalian galanin generally inhibited the secretion of SS-25, but stimulated the release of SS-14 at 10(-7) M in the presence of 3 mM glucose. These results suggest that CCK, NPY and galanin modulate the release of the somatostatins present within the trout pancreas. Furthermore, glucose may mediate the overall responsiveness of somatostatin-secreting cells to these peptides.