We previously reported that the BB diabetic rat is characterized by a reduction in pancreatic immunoreactive somatostatin (SLI) content, δ-cell mass, and δ-cell secretory reserve. Despite this, portal plasma SLI levels are elevated in diabetic animals and normalized by insulin therapy. These findings comprise indirect evidence for SLI hypersecretion by the gut in untreated BB rats. This study was undertaken with isolated stomach perfusions to investigate directly the secretory status of gastric δ-cells in this diabetic model. Isolated stomachs of three groups of insulin-treated diabetic, untreated diabetic, and nondiabetic control rats were perfused in situ under basal and glucagon-stimulated (5 nM) conditions. Untreated diabetic BB rats exhibited significant enhancement of basal and glucagonstimulated gastric SLI release. Insulin treatment reduced gastric SLI release to significantly subnormal levels. More than 95% of basal and stimulated SLI released in diabetic BB and normal control rats coeluted with synthetic somatostatin-14 on Sephadex G-50 columns. We conclude that 1) basal and stimulated gastric SLI release is increased in untreated BB rats and is suppressed with insulin therapy, 2) gastric δ-cell hyperfunction accounts for portal vein hypersomatostatinemia characteristic of untreated diabetic BB rats, and 3) somatostatin-14 is the main molecular form of SLI released from normal and diabetic stomachs.

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