Effects of K+and Arginine on Insulin, Glucagon, and Somatostatin Release from the in Vitro Perfused Rat Pancreas*
Barbara J. Frankel, Anneliese Heldt, Gerold M. Grodsky
Abstract
Barbara J. Frankel, Anneliese Heldt, Gerold M. Grodsky
Abstract
Rat pancreases were perfused in vitro for 5-min periods with K+ alone (8, 10, and 12 mM) or in the presence of arginine (10 mM). Alone, K+ caused bursts of insulin, glucagon, and somatostatin (SRIF) release; with arginine, it caused a burst of insulin and sustained SRIF release, but caused sustained suppression of glucagon. This suppression correlated better with SRIF than insulin release. Therefore, if a paracrine effect is responsible for the inhibition of glucagon secretion under these circumstances, SRIF is a more likely candidate than insulin.
OpenAlex reports 11 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Rat pancreases were perfused in vitro for 5-min periods with K+ alone (8, 10, and 12 mM) or in the presence of arginine (10 mM). Alone, K+ caused bursts of insulin, glucagon, and somatostatin (SRIF) release; with arginine, it caused a burst of insulin and sustained SRIF release, but caused sustained suppression of glucagon. This suppression correlated better with SRIF than insulin release. Therefore, if a paracrine effect is responsible for the inhibition of glucagon secretion under these circumstances, SRIF is a more likely candidate than insulin.
Key concepts: Internal medicine, Glucagon, Endocrinology, Somatostatin, Insulin, Pancreas, Arginine, In vitro