TY - JOUR
T1 - Somatostatin induced changes in insulin and glucagon secretion in normal and diabetic dogs
AU - Sakurai, H.
AU - Dobbs, R.
AU - Unger, Roger H
PY - 1974
Y1 - 1974
N2 - In conscious dogs iv infused somatostatin (3.3 μg per min for 1 hr) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 μg per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. Consistent bihormonal suppression occurred at rates as low as 24 ng per kg per min, but was variable at 12 and 2.4 ng per kg per min. When somatostatin induced (3.3 μg per min) hypoglucagonemia was corrected by exogenous glucagon, hyperglycemia occurred. In dogs with long standing insulin requiring alloxan diabetes 3.3 μg per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30 min infusion and lowered glucose by 36.4 ± 6.1 mg per dl, about 1 mg per dl per min. Glucagon suppression was maintained despite alanine infusion, and glucose, which rose 29 mg per dl during alanine infusion without somatostatin, declined 58 mg per dl in the somatostatin treated diabetic dogs despite alanine. Continuous infusion of somatostatin for 24 hr in five insulin requiring alloxan diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. Hyperglycemia occurs during somatostatin induced insulin lack only if hypoglucagonemia is corrected. Somatostatin suppresses glucagon in diabetic dogs and lowers their plasma glucose approximately 1 mg per dl per min, even when the gluconeogenic substrate alanine is abundant. Glucagon suppression can be maintained for several hours in such dogs and hyperglycemia is thereby reduced.
AB - In conscious dogs iv infused somatostatin (3.3 μg per min for 1 hr) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 μg per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. Consistent bihormonal suppression occurred at rates as low as 24 ng per kg per min, but was variable at 12 and 2.4 ng per kg per min. When somatostatin induced (3.3 μg per min) hypoglucagonemia was corrected by exogenous glucagon, hyperglycemia occurred. In dogs with long standing insulin requiring alloxan diabetes 3.3 μg per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30 min infusion and lowered glucose by 36.4 ± 6.1 mg per dl, about 1 mg per dl per min. Glucagon suppression was maintained despite alanine infusion, and glucose, which rose 29 mg per dl during alanine infusion without somatostatin, declined 58 mg per dl in the somatostatin treated diabetic dogs despite alanine. Continuous infusion of somatostatin for 24 hr in five insulin requiring alloxan diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. Hyperglycemia occurs during somatostatin induced insulin lack only if hypoglucagonemia is corrected. Somatostatin suppresses glucagon in diabetic dogs and lowers their plasma glucose approximately 1 mg per dl per min, even when the gluconeogenic substrate alanine is abundant. Glucagon suppression can be maintained for several hours in such dogs and hyperglycemia is thereby reduced.
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U2 - 10.1172/JCI107886
DO - 10.1172/JCI107886
M3 - Article
C2 - 4436439
AN - SCOPUS:0016176118
SN - 0021-9738
VL - 54
SP - 1395
EP - 1402
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 6
ER -