TY - JOUR
T1 - Dissociation of glucose stimulation of somatostatin and insulin release from glucose inhibition of glucagon release in the isolated perfused rat pancreas
AU - Sorenson, R. L.
AU - Elde, R. P.
PY - 1983
Y1 - 1983
N2 - This study investigated the modulating role of glucose on 5 mM arginine stimulation of insulin, somatostatin, and glucagon release from the isolated perfused rat pancreas. As the concentration of glucose was increased linearly from 50 to 300 mg/dl, arginine-stimulated glucagon release was inhibited, with half-maximal inhibition occurring at 84 mg/dl glucose. As glucose increased above 80 mg/dl, somatostatin and insulin release was initiated and they continued to increase in a nearly parallel fashion during the glucose gradient (300 mg/dl). When 5 mM arginine was presented 'en block' against varying backgrounds of glucose (30, 60, 75, 90, 120, 150, and 300 mg/dl), glucagon release was diminished in the presence of glucose concentrations greater than 50 mg/dl. Arginine elicited insulin release at all glucose concentrations and was significantly augmented in the presence of glucose greater than 90 mg/dl. Arginine-stimulated somatostatin release was detectable in the 90-mg/dl glucose group and was significantly augmented in the 120- and 150-mg/dl glucose treatment groups. In conclusion, these studies indicate that glucose modulates the arginine effect on alpha, beta, and delta cells; and alpha cells have a lower threshold to glucose than beta and delta cells. Glucose inhibits arginine-stimulated glucagon release in the absence of a detectable glucose or arginine stimulation of somatostatin release. Thus, glucose appears to play a major role in the control of the putative hormonal influence among the islet cells.
AB - This study investigated the modulating role of glucose on 5 mM arginine stimulation of insulin, somatostatin, and glucagon release from the isolated perfused rat pancreas. As the concentration of glucose was increased linearly from 50 to 300 mg/dl, arginine-stimulated glucagon release was inhibited, with half-maximal inhibition occurring at 84 mg/dl glucose. As glucose increased above 80 mg/dl, somatostatin and insulin release was initiated and they continued to increase in a nearly parallel fashion during the glucose gradient (300 mg/dl). When 5 mM arginine was presented 'en block' against varying backgrounds of glucose (30, 60, 75, 90, 120, 150, and 300 mg/dl), glucagon release was diminished in the presence of glucose concentrations greater than 50 mg/dl. Arginine elicited insulin release at all glucose concentrations and was significantly augmented in the presence of glucose greater than 90 mg/dl. Arginine-stimulated somatostatin release was detectable in the 90-mg/dl glucose group and was significantly augmented in the 120- and 150-mg/dl glucose treatment groups. In conclusion, these studies indicate that glucose modulates the arginine effect on alpha, beta, and delta cells; and alpha cells have a lower threshold to glucose than beta and delta cells. Glucose inhibits arginine-stimulated glucagon release in the absence of a detectable glucose or arginine stimulation of somatostatin release. Thus, glucose appears to play a major role in the control of the putative hormonal influence among the islet cells.
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U2 - 10.2337/diabetes.32.6.561
DO - 10.2337/diabetes.32.6.561
M3 - Article
C2 - 6138289
AN - SCOPUS:0020623078
SN - 0012-1797
VL - 32
SP - 561
EP - 567
JO - Diabetes
JF - Diabetes
IS - 6 I
ER -