[Speculation] is the food-noise effect central, peripheral, or both
Trying to get a straight answer on this: is the food-noise effect central, peripheral, or both. The half-life explanation was the thing that made weekly dosing intuitive for me rather than arbitrary. Was completely wrong about the gastric emptying story in a thread here two years ago. Someone corrected me with a…
Speculation is welcome here if it is labelled. This one has been relabelled rather than removed.
Went looking for human data on a mechanism everybody here asserts. Found preclinical work and one small study. That was clarifying.
This. Albumin binding and modification are why the half-life is what it is, and it is a design decision rather than an accident.
This.
This is the concept everything else on this board is downstream of.
Is that from a human study or a preclinical model?
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.
Read the primary paper after arguing about the summary for a fortnight.
Agreed — and it is why the central and peripheral stories are complementary rather than rival.
The incretin effect is the observation that oral glucose provokes a larger insulin response than intravenous glucose at matched glycaemia, and the difference is mediated by gut hormones. That is the foundation the whole class sits on.