incretin: what the trials say vs what this community says
incretin: what the trials say vs what this community says. Making the case below, and I expect to lose some of it in the comments. 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…
Receptor expression in a tissue is necessary but not sufficient for an effect. You also need the agonist to reach it at relevant exposure, and that is where a lot of confident mechanism talk falls down.
Receptor expression in a tissue is necessary but not sufficient for an effect.
Agreed — and it is why the central and peripheral stories are complementary rather than rival.
Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.
Correction: that is glucose-dependent insulin secretion, which is why hypoglycaemia risk is low as monotherapy. Not the same claim as you made.
incretin effect first, then everything else in this board makes sense
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.
receptor agonism is not the same as receptor activation in every tissue