Synthalin::a lost lesson for glucagon suppression in diabetes therapeutics

Abstract

Objectives Within mammalian pancreatic islets, there are two major endocrine cell types, beta-cells which secrete insulin and alpha-cells which secrete glucagon. Whereas, insulin acts to lower circulating glucose, glucagon counters this by increasing circulating glucose via the mobilisation of glycogen. Synthalin A (Syn A) was the subject of much research in the 1920s and 1930s as a potential pancreatic alpha-cell toxin to block glucagon secretion. However, with the discovery of insulin and its lifesaving use in patients with diabetes, research on Syn-A was discontinued. Key findings This short review looks back on early studies performed with Syn A in animals and humans with diabetes. These are relevant today because both type 1 and type 2 diabetes are now recognised as states of not only insulin deficiency but also glucagon excess. Summary Lessons learned from this largely forgotten portfolio of work and therapeutic strategy aimed at limiting the number or function of islet alpha-cells might be worthy of reconsideration.

Publication DOI: https://doi.org/10.1093/jpp/rgad010
Divisions: College of Health & Life Sciences
Additional Information: Copyright © The Author(s) 2023. Published by Oxford University Press on behalf of the Royal Pharmaceutical Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
Uncontrolled Keywords: Synthalin (Syn),alpha-cells,beta-cells,diabetes,glucagon,pancreatic islets,Medicine(all)
Publication ISSN: 2042-7158
Last Modified: 28 Mar 2024 08:23
Date Deposited: 16 Mar 2023 10:00
Full Text Link:
Related URLs: https://academi ... 766?login=false (Publisher URL)
http://www.scop ... tnerID=8YFLogxK (Scopus URL)
PURE Output Type: Article
Published Date: 2023-06
Published Online Date: 2023-03-04
Accepted Date: 2023-01-25
Authors: Thomas, Keith G
Klempel, Natalie J
Flatt, Peter R
Bailey, Clifford J (ORCID Profile 0000-0002-6998-6811)
Moffett, R Charlotte

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