GLP-1 receptor distribution: central and peripheral — one year on

GLP-1 receptor distribution: central and peripheral — one year on — setting out what I have, and where I think it stops being reliable.

An honest uncertainty about GLP-1 receptor distribution rather than a disguised assertion.

I do not know the answer and I have not been able to find one. What I have is the shape of the question, which may be worth more than my guess at the answer.

Picking up post #2: that is the part I would want checked first.

Glucagon receptor agonism: glucagon receptor agonism increases energy expenditure and promotes hepatic fat oxidation. The mechanism is distinct from GLP-1 and GIP agonism and the clinical consequences are still being characterised.

Signalling through cyclic AMP is the canonical pathway and is not the only one. Beta-arrestin recruitment differs between ligands and its clinical significance here is unestablished.

It is one reading of the data and not the only reasonable one.

GLP-1 receptor agonism produces its metabolic effects through more than one route: central satiety signalling, delayed gastric emptying, and glucose-dependent insulin secretion. Attributing everything to one of them is where most simplified accounts go wrong.

That is a description of practice, not a recommendation of it.

The area postrema sits outside the blood-brain barrier and is where a great deal of the nausea signalling in this class originates. That is why the effect is central and not gastric irritation.

Adding a source would improve this post and I do not have one to hand.