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Acetylcholine Stimulates Insulin, Glucagon, and Somatostatin Release in the Perfused Chicken Pancreas*

Richard N. Honey, GORDON C. WEIRf

Open publisher page 41 citations

Abstract

To evaluate the possible cholinergic control of islet hormone secretion, acetylcholine (10 microM) was perfused into the isolated chicken pancreas-duodenum, with perfusate concentrations of 2.8, 14, or 42 mM glucose. Prompt and significant stimulation of insulin, glucagon, and somatostatin secretion was seen when the glucose concentration was 14 mM, and this stimulation was blocked by preinfusion of atropine sulfate (50 microM). Similar stimulation of all three peptides was seen when the perfusate concentration of glucose was 42 mM. When the perfusate glucose concentration was 2.8 mM, the insulin response to acetylcholine was absent and the response by glucagon could not be discerned, perhaps because release was close to maximal. The somatostatin response, however, was only slightly diminished from that seen at higher glucose levels. The B cell response to acetycholine in the chicken was considerably greater than the weak responses seen to high glucose or arginine, suggesting a dominant role for cholinergic control of avian insulin secretion. In addition, the parasympathetic nervous system may also play a role in the secretory control of A- and D cells.

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What this paper is about

To evaluate the possible cholinergic control of islet hormone secretion, acetylcholine (10 microM) was perfused into the isolated chicken pancreas-duodenum, with perfusate concentrations of 2.8, 14, or 42 mM glucose. Prompt and significant stimulation of insulin, glucagon, and somatostatin secretion was seen when the glucose concentration was 14 mM, and this stimulation was blocked by preinfusion of atropine sulfate (50 microM). Similar stimulation of all three peptides was seen when the perfusate concentration of glucose was 42 mM. When the perfusate glucose concentration was 2.8 mM, the insulin response to acetylcholine was absent and the response by glucagon could not be discerned, perhaps because release was close to maximal. The somatostatin response, however, was only slightly diminished from that seen at higher glucose levels. The B cell response to acetycholine in the chicken was considerably greater than the weak responses seen to high glucose or arginine, suggesting a dominant role for cholinergic control of avian insulin secretion. In addition, the parasympathetic nervous system may also play a role in the secretory control of A- and D cells.

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Available abstract

To evaluate the possible cholinergic control of islet hormone secretion, acetylcholine (10 microM) was perfused into the isolated chicken pancreas-duodenum, with perfusate concentrations of 2.8, 14, or 42 mM glucose. Prompt and significant stimulation of insulin, glucagon, and somatostatin secretion was seen when the glucose concentration was 14 mM, and this stimulation was blocked by preinfusion of atropine sulfate (50 microM). Similar stimulation of all three peptides was seen when the perfusate concentration of glucose was 42 mM. When the perfusate glucose concentration was 2.8 mM, the insulin response to acetylcholine was absent and the response by glucagon could not be discerned, perhaps because release was close to maximal. The somatostatin response, however, was only slightly diminished from that seen at higher glucose levels. The B cell response to acetycholine in the chicken was considerably greater than the weak responses seen to high glucose or arginine, suggesting a dominant role for cholinergic control of avian insulin secretion. In addition, the parasympathetic nervous system may also play a role in the secretory control of A- and D cells.

Key concepts: Internal medicine, Endocrinology, Somatostatin, Glucagon, Insulin, Acetylcholine, Pancreas, Pancreatic hormone

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Acetylcholine Stimulates Insulin, Glucagon, and Somatostatin Release in the Perfused Chicken Pancreas* — Research Paper | ScholarLens