why does nobody talk about appetite
Genuine question, and the title is the question: why does nobody talk about appetite. Spent an evening on the receptor distribution literature and the side-effect map suddenly stopped looking random. Read the primary paper after arguing about the summary for a fortnight. The discussion section said almost the…
GIP receptor biology is genuinely unsettled — there is a live argument about agonism versus antagonism at the receptor — and the clinical results are robust regardless, which is an uncomfortable and interesting position.
GIP receptor biology is genuinely unsettled — there is a live argument about agonism versus antagonism at the receptor — and the clinical results are
This is the concept everything else on this board is downstream of.
Right — mechanism gives you a direction. It never gives you an effect size and people use it as though it does.
I would not read that in vitro number across to a person. The conditions are nothing like physiological.
Asked a question here that I thought was stupid and got three papers back. Best thread I have been in on this site.
Started reading limitations sections first. It has changed how much weight I give to almost everything posted here.
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.
Which receptor arm are you attributing that to?
Does the effect persist with continued dosing or does tolerance develop?
mechanism explains a direction, not a magnitude
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.
Are we talking about receptor affinity or clinical potency?
the peripheral and central stories are not in competition