[Discussion] can we stop arguing about appetite until somebody posts a number
Question in the title, detail here: can we stop arguing about appetite until somebody posts a number.
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.
Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.
Long half-life in this class comes from structural modification that promotes albumin binding and resists enzymatic degradation. Weekly dosing is a consequence of the molecule, not a convenience decision.
Would rather be corrected in public than confident in private.
best — the order this archive was captured in
Left up and flaired Explainer. This is the standard of post the board was created for.
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.
Correction: that is glucose-dependent insulin secretion, which is why hypoglycaemia risk is low as monotherapy. Not the same claim as you made.
Went looking for human data on a mechanism everybody here asserts. Found preclinical work and one small study. That was clarifying.
Yes. The discussion section is where the authors say what they actually think, and almost nobody here reads it.
Does the effect persist with continued dosing or does tolerance develop?
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.
Tolerance to the gastric effect develops with continued exposure while the appetite effect largely persists.
Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.
Asked a question here that I thought was stupid and got three papers back. Best thread I have been in on this site.
Agreed — the incretin effect is the load-bearing concept and everything downstream reads differently once you have it.
Are we talking about receptor affinity or clinical potency?
- 1Left up and flaired Explainer. This is the standard of post the board was…7 comments in this branch · started by u/incretin_ivy