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Published on: November 16, 2011
Synthalin: a lost lesson for glucagon suppression in diabetes therapeutics
Keith G Thomas1, Natalie J Klempel1, Peter R Flatt1
1SAAD Centre for Pharmacy and Diabetes, Ulster University, Coleraine, Northern Ireland, UK.
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.
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