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.

• Authors: Keith G Thomas, Natalie J Klempel, Peter R Flatt, Clifford J Bailey, R Charlotte Moffett
• Journal: The Journal of pharmacy and pharmacology (J Pharm Pharmacol) Vol. 75 Issue 6 Pg. 758-763 (Jun 05 2023) ISSN: 2042-7158 [Electronic] England
• PMID: 36879406 (Publication Type: Journal Article)
• Copyright: © The Author(s) 2023. Published by Oxford University Press on behalf of the Royal Pharmaceutical Society.

Chemical References

• Glucagon
• Insulin
• Glucose

Topics

• Animals
• Humans
• Glucagon (metabolism)
• Diabetes Mellitus, Type 2 (drug therapy, metabolism)
• Insulin (metabolism)
• Islets of Langerhans (metabolism)
• Glucose (metabolism)
• Mammals (metabolism)