Origin of peripheral venous hypersomatostatinemia in alloxan-diabetic dogs.

Abstract

Basal and postprandial somatostatin-like immunoreactivity (SLI) is elevated in the peripheral venous plasma of chronic alloxan-diabetic dogs. To determine if this hypersomatostatinemia was the consequence of increased somatostatin release from the pancreas, stomach, or both, plasma SLI was measured in the pancreaticoduodenal, antral, and fundic veins and in the inferior vena cava in response to stimulation by a gastric liver test meal, followed by an intragastric HCl load. Basal and postprandial inferior vena caval plasma SLI levels were significantly higher than the control level (P less than 0.05-0.001), confirming earlier findings. Basal pancreatic venous SLI was 780 +/- 45 pg/ml in the diabetic dogs and 493 +/- 65 pg/ml in the controls (P less than 0.02). In response to the liver meal at pH 7, the incremental pancreatic venous SLI level in the diabetic dogs was 1630 +/- 95 pg/ml, and after HCl it rose to 9479 +/- 384 pg/ml compared to 938 +/- 80 and 4677 +/- 192 pg/ml, respectively, in the controls (P less than 0.02 and P less than 0.005). However, antral and fundic venous SLI levels in the diabetic dogs did not differ from the controls in either basal or stimulated states. The present data demonstrate that the pancreas and not the stomach is the probable source of the peripheral hypersomatostatinemia of alloxan-diabetic dogs.