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.
| Original language | English |
|---|---|
| Pages (from-to) | 758-763 |
| Number of pages | 6 |
| Journal | Journal of Pharmacy and Pharmacology |
| Volume | 75 |
| Issue number | 6 |
| Early online date | 4 Mar 2023 |
| DOIs | |
| Publication status | Published - Jun 2023 |
Bibliographical note
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.
Keywords
- Synthalin (Syn)
- alpha-cells
- beta-cells
- diabetes
- glucagon
- pancreatic islets