1983EndocrinologyRequires access

Effect of Spontaneous Diabetes on Hormone Release in BB/Phi Rats: Comparison between the Isolated Perfused Pancreas/Stomach/Duodenum/Spleen and the Isolated Perfused Pancreas*

G. Boden, Ali Naji, Clyde F. Barker, V. JUNE, Franz M. Matschinsky

Open publisher page 3 citations

Abstract

We have studied the effects of spontaneous diabetes in BB/Phi rats on hormone release in response to amino acids (15 mM) and to amino acids (15 mM) plus glucose (10 mM) from isolated perfused pancreas/stomach/duodenum/spleen (PSDS) and from isolated perfused pancreas (P) preparations. In the PSDS preparation, diabetes reduced total integrated insulin output by 97% (from 1146 +/- 198 to 40 +/- 24 ng/65 min, P less than 0.001), and glucagon output by about 50% (from 51.6 +/- 13.1 to 24.0 +/- 3.7 ng/65 min, P less than 0.05), whereas somatostatin output did not change (105.5 +/- 48.1 to 110.1 +/- 36.9 ng/65 min). In the P preparation, integrated glucagon output fell by 91% (from 97.9 +/- 26.8 to 8.6 +/- 4.8 ng/65 min, P less than 0.01) whereas integrated somatostatin output more than doubled (from 28.1 +/- 7.5 to 69.6 +/- 14.2 ng/65 min, P less than 0.05). Intestinal glucagon and somatostatin contributions were estimated by comparing hormone release from the PSDS with that from the P preparations. We conclude that in our nondiabetic BB/Phi rats, the pancreas was the only source for the release of glucagon and that the intestinal tract secreted more somatostatin than the pancreas. In the diabetic BB/Phi rats, pancreatic glucagon and insulin release was virtually abolished while glucagon secretion from the intestinal tract increased and somatostatin secretion decreased.

About this research paper

What this paper is about

We have studied the effects of spontaneous diabetes in BB/Phi rats on hormone release in response to amino acids (15 mM) and to amino acids (15 mM) plus glucose (10 mM) from isolated perfused pancreas/stomach/duodenum/spleen (PSDS) and from isolated perfused pancreas (P) preparations. In the PSDS preparation, diabetes reduced total integrated insulin output by 97% (from 1146 +/- 198 to 40 +/- 24 ng/65 min, P less than 0.001), and glucagon output by about 50% (from 51.6 +/- 13.1 to 24.0 +/- 3.7 ng/65 min, P less than 0.05), whereas somatostatin output did not change (105.5 +/- 48.1 to 110.1 +/- 36.9 ng/65 min). In the P preparation, integrated glucagon output fell by 91% (from 97.9 +/- 26.8 to 8.6 +/- 4.8 ng/65 min, P less than 0.01) whereas integrated somatostatin output more than doubled (from 28.1 +/- 7.5 to 69.6 +/- 14.2 ng/65 min, P less than 0.05). Intestinal glucagon and somatostatin contributions were estimated by comparing hormone release from the PSDS with that from the P preparations. We conclude that in our nondiabetic BB/Phi rats, the pancreas was the only source for the release of glucagon and that the intestinal tract secreted more somatostatin than the pancreas. In the diabetic BB/Phi rats, pancreatic glucagon and insulin release was virtually abolished while glucagon secretion from the intestinal tract increased and somatostatin secretion decreased.

Why it matters

OpenAlex reports 3 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

We have studied the effects of spontaneous diabetes in BB/Phi rats on hormone release in response to amino acids (15 mM) and to amino acids (15 mM) plus glucose (10 mM) from isolated perfused pancreas/stomach/duodenum/spleen (PSDS) and from isolated perfused pancreas (P) preparations. In the PSDS preparation, diabetes reduced total integrated insulin output by 97% (from 1146 +/- 198 to 40 +/- 24 ng/65 min, P less than 0.001), and glucagon output by about 50% (from 51.6 +/- 13.1 to 24.0 +/- 3.7 ng/65 min, P less than 0.05), whereas somatostatin output did not change (105.5 +/- 48.1 to 110.1 +/- 36.9 ng/65 min). In the P preparation, integrated glucagon output fell by 91% (from 97.9 +/- 26.8 to 8.6 +/- 4.8 ng/65 min, P less than 0.01) whereas integrated somatostatin output more than doubled (from 28.1 +/- 7.5 to 69.6 +/- 14.2 ng/65 min, P less than 0.05). Intestinal glucagon and somatostatin contributions were estimated by comparing hormone release from the PSDS with that from the P preparations. We conclude that in our nondiabetic BB/Phi rats, the pancreas was the only source for the release of glucagon and that the intestinal tract secreted more somatostatin than the pancreas. In the diabetic BB/Phi rats, pancreatic glucagon and insulin release was virtually abolished while glucagon secretion from the intestinal tract increased and somatostatin secretion decreased.

Key concepts: Internal medicine, Endocrinology, Somatostatin, Glucagon, Duodenum, Pancreas, Insulin, Hormone

Related papers

Back to paper searchBrowse research topicsOriginal source
Effect of Spontaneous Diabetes on Hormone Release in BB/Phi Rats: Comparison between the Isolated Perfused Pancreas/Stomach/Duodenum/Spleen and the Isolated Perfused Pancreas* — Research Paper | ScholarLens