A possible role of the pancreatic α1- and α2-cells as local regulators of insulin secretion

Bo Hellman, Å. Lernmark

Research output: Chapter in Book/Report/Conference proceedingBook chapterResearchpeer-review

Abstract

In addition to a majority of insulin-producing β-cells, the mammalian pancreatic islets contain considerable numbers of α1- and α2-cells. While the α2-cells are the cellular source of glucagon, the secretory product stored in the granules of the α1-cells still remains to be identified.

Several authors have reported that glucagon stimulates insulin release. This effect of glucagon was found to be dependent on the presence of adequate amounts of glycogen in the β-cells. The resulting insensitivity of the β-cells to glucagon under conditions of hypoglycemia is consistent with the previous concept of glucagon as a local regulator of the β-cell function.

The α1-cells may also be considered as possible regulators of insulin secretion from the adjacent β-cells. The α1-cells are morphologically even more closely related to the β-cells than are the α2-cells. After measuring the amounts of insulin secreted from microdissected mouse islets under different experimental conditions it could be concluded that there exists at least one inhibitor of insulin release within the pancreatic islets. Such an inhibitor is probably located to the α1-cells, as shown by the fact that a water extract of pigeon α1-cells significantly reduced the amounts of insulin secreted in vitro. The supposed inhibitor of insulin release in the pancreatic α1-cells may be identical with gastrin, which inhibits the glucose-stimulated insulin release when tested at a concentration of only 0.15 μg/ml.
Original languageEnglish
Title of host publicationThe Structure and Metabolism of the Pancreatic Islets
Subtitle of host publicationA Centennial of Paul Langerhans' Discovery
EditorsSture Falkmer, Bo Hellman, Inge-Bert Täljedal
Place of PublicationOxford
PublisherPergamon Press Ltd.
Pages453-462
ISBN (Print)978-0-08-015844-0
DOIs
Publication statusPublished - 1970
Externally publishedYes

Subject classification (UKÄ)

  • Endocrinology and Diabetes

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