[Paper] amylin co-agonism is genuinely different pharmacology, not just more GLP-1
amylin co-agonism is genuinely different pharmacology, not just more GLP-1. I have gone back and forth on this for months. The mental model, in four steps, that makes the rest of this site legible. One: gut hormones amplify the insulin response to food. Two: agonists at those receptors act peripherally on insulin…
GLP-1 receptor agonism acts both peripherally — insulin secretion in a glucose-dependent way, slowed gastric emptying — and centrally, on appetite regulation. The central component is the better explanation for sustained intake reduction.
What was the exposure in that experiment relative to therapeutic?
What was the exposure in that experiment relative to therapeutic?
Adding the caveat the paper itself makes in its limitations section, which is stronger than anything in this thread.
That study was in a rodent model. Worth stating, since the thread has been reading it as human data.
Yes. The central component is the one that explains the reports on this site better than gastric emptying does.
preclinical is not clinical and rodents are not small people
gastric emptying slows, it does not stop
preclinical is not clinical and rodents are not small people
This is the concept everything else on this board is downstream of.
The half-life explanation was the thing that made weekly dosing intuitive for me rather than arbitrary.
the central appetite effect is doing more work than the gut effect