[PSA] gastric emptying is not what most of this community thinks it is
Short public-service post: gastric emptying is not what most of this community thinks it is. 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…
Was completely wrong about the gastric emptying story in a thread here two years ago. Someone corrected me with a citation and I have not made that mistake since.
Disagree. That is a preclinical finding in a rodent model and you are stating it as human pharmacology.
Disagree.
Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.
a mechanism you can state is not a mechanism you have demonstrated
albumin binding is most of the half-life story
Tolerance to the gastric effect develops with continued exposure while the appetite effect largely persists. That single fact explains most of the "it settles but it still works" pattern the side-effect board reports.
the central appetite effect is doing more work than the gut effect
GIP is the arm people argue about because the biology is genuinely unsettled
Asked a question here that I thought was stupid and got three papers back. Best thread I have been in on this site.
Cosigning on GIP. The genuinely interesting thing is that the biology is not settled and the clinical result is nonetheless robust.
Correction: that is glucose-dependent insulin secretion, which is why hypoglycaemia risk is low as monotherapy. Not the same claim as you made.