TY - JOUR
T1 - Origin of peripheral venous hypersomatostatinemia in alloxan-diabetic dogs
AU - Schusdziarra, V.
AU - Rouiller, D.
AU - Harris, V.
AU - Unger, Roger H
PY - 1981/10
Y1 - 1981/10
N2 - 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 HC1 load. Basal and postprandial inferior vena caval plasma SLI levels were significantly higher than the control level (p < 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 < 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 HC1 it rose to 9479± 384 pg/ml compared to 938± 80 and 4677± 192 pg/, respectively, in the controls (p< 0.02 and p < 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.
AB - 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 HC1 load. Basal and postprandial inferior vena caval plasma SLI levels were significantly higher than the control level (p < 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 < 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 HC1 it rose to 9479± 384 pg/ml compared to 938± 80 and 4677± 192 pg/, respectively, in the controls (p< 0.02 and p < 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.
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U2 - 10.1210/endo-109-4-1107
DO - 10.1210/endo-109-4-1107
M3 - Article
C2 - 6116595
AN - SCOPUS:0019404152
SN - 0013-7227
VL - 109
SP - 1107
EP - 1110
JO - Endocrinology
JF - Endocrinology
IS - 4
ER -