Synthalin: a lost lesson for glucagon suppression in diabetes therapeutics

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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 languageEnglish
Pages (from-to)758-763
Number of pages6
JournalJOURNAL OF PHARMACY AND PHARMACOLOGY
Volume75
Issue number6
Early online date4 Mar 2023
DOIs
Publication statusPublished (in print/issue) - 5 Jun 2023

Bibliographical note

Funding Information:
This area of research was supported by the award of Ulster University Vice-Chancellor PhD Research Scholarship to N.K.

Publisher Copyright:
© 2023 The Author(s). Published by Oxford University Press on behalf of the Royal Pharmaceutical Society.

Keywords

  • Synthalin (Syn)
  • glucagon
  • diabetes
  • beta-cells
  • pancreatic islets
  • alpha-cells

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