RESUMEN
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.