1993Hormone and Metabolic ResearchRequires access

Effects of Amylin on the Release of Insulin and Glucagon from the Perfused Rat Pancreas

Kaoru Inoue, S. Hiramatsu, Akitaka Hisatomi, F. Umeda, Hajime Nawata

Open publisher page 21 citations

Abstract

Amylin is a normal secretory protein of the pancreatic beta-cells as well as a major constituent of the islet amyloid deposits in patients with non-insulin-dependent diabetes mellitus. We studied the effects of amylin on the release of insulin and glucagon from the isolated perfused rat pancreas. Rat amylin was dissolved in basal perfusates to a final concentration of 100 nM. Amylin did not alter glucose-stimulated secretion of insulin but significantly inhibited arginine-stimulated secretion of insulin (control: 20.9 +/- 1.4 pmol/min; amylin group: 14.8 +/- 1.6 pmol/min, p < 0.05). Amylin did not alter the release of glucagon from the perfused rat pancreas in response to 16.7 mM glucose and 10 mM arginine. These findings suggest that amylin may modulate the secretion of insulin from pancreatic beta-cells.

About this research paper

What this paper is about

Amylin is a normal secretory protein of the pancreatic beta-cells as well as a major constituent of the islet amyloid deposits in patients with non-insulin-dependent diabetes mellitus. We studied the effects of amylin on the release of insulin and glucagon from the isolated perfused rat pancreas. Rat amylin was dissolved in basal perfusates to a final concentration of 100 nM. Amylin did not alter glucose-stimulated secretion of insulin but significantly inhibited arginine-stimulated secretion of insulin (control: 20.9 +/- 1.4 pmol/min; amylin group: 14.8 +/- 1.6 pmol/min, p < 0.05). Amylin did not alter the release of glucagon from the perfused rat pancreas in response to 16.7 mM glucose and 10 mM arginine. These findings suggest that amylin may modulate the secretion of insulin from pancreatic beta-cells.

Why it matters

OpenAlex reports 21 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Amylin is a normal secretory protein of the pancreatic beta-cells as well as a major constituent of the islet amyloid deposits in patients with non-insulin-dependent diabetes mellitus. We studied the effects of amylin on the release of insulin and glucagon from the isolated perfused rat pancreas. Rat amylin was dissolved in basal perfusates to a final concentration of 100 nM. Amylin did not alter glucose-stimulated secretion of insulin but significantly inhibited arginine-stimulated secretion of insulin (control: 20.9 +/- 1.4 pmol/min; amylin group: 14.8 +/- 1.6 pmol/min, p < 0.05). Amylin did not alter the release of glucagon from the perfused rat pancreas in response to 16.7 mM glucose and 10 mM arginine. These findings suggest that amylin may modulate the secretion of insulin from pancreatic beta-cells.

Key concepts: Amylin, Internal medicine, Endocrinology, Insulin, Glucagon, Arginine, Pancreas, Pancreatic hormone

Related papers

Back to paper searchBrowse research topicsOriginal source
Effects of Amylin on the Release of Insulin and Glucagon from the Perfused Rat Pancreas — Research Paper | ScholarLens