mechanism is the most under-discussed thing on this board
The title is the argument: mechanism is the most under-discussed thing on this board. Here is the rest of it. Went looking for human data on a mechanism everybody here asserts. Found preclinical work and one small study. That was clarifying. Tried to build a mental model from mechanism alone and produced a confident…
Is there any human data on that mechanism yet?
Does the effect persist with continued dosing or does tolerance develop?
dose response is not linear and nobody should assume it is
incretin effect first, then everything else in this board makes sense
Read the primary paper after arguing about the summary for a fortnight. The discussion section said almost the opposite of what the thread had concluded.
a mechanism you can state is not a mechanism you have demonstrated
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.
That study was in a rodent model. Worth stating, since the thread has been reading it as human data.
Spent an evening on the receptor distribution literature and the side-effect map suddenly stopped looking random.
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.
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.