Platypus venom could hold the key to the future of diabetes treatment
Researchers at the University of Adelaide in Australia have found that a longer-lasting form of the hormone glucagon-like peptide-1 (GLP-1) – which promotes the release of insulin, lowering blood sugar levels – in platypus venom. This discovery could pave the way for new treatments for type 2 diabetes in humans.
GLP-1 is normally secreted in the gut of both humans and animals, but it typically degrades within minutes.
The males of the extraordinary semi-aquatic mammal – one of the only kind to lay eggs – have venomous spurs on its hind limbs for delivering venom to its competitors during mating season.
Lead researcher Frank Grutzner said his team was surprised to find the hormone was produced not only in the platypus’ gut, but also in its venom.
“We’ve found that GLP-1 is degraded in monotremes (platypus, echidna) by a completely different mechanism,” Professor Grutzner said.
Echidnas, also known as spiny anteaters – another iconic Australian species – were also found to carry the unusual hormone.
They are not the only animals to use insulin against enemies. The gila monster, a venomous lizard native to the US and Mexico, and the geographer cone, a dangerous sea snail which can kill entire schools of fish by releasing insulin into the sea, both also weaponize the chemical.
“Further analysis of the genetics of monotremes reveals that there seems to be a kind of molecular warfare going on between the function of GLP-1, which is produced in the gut, but also surprisingly in their venom.”
Associate Professor Briony Forbes said the two different functions of GLP-1 in the platypus — in the gut as a regulator of blood glucose, and in the venom to fend off other males — have seen the hormone evolve.
“The function in venom has most likely triggered the evolution of a stable form of GLP-1 in monotremes,” she said.”Excitingly, stable GLP-1 molecules are highly desirable as potential type 2 diabetes treatments.”
“I think the next step is really to do some experiments in an established medical animal system like the mouse for example, and study how that variant is working in that mouse model and take it from there,” Grutzner said.
He emphasized that much more research was needed before the discovery could, if ever, lead to a human treatment
