three years of appetite threads, summarised so you do not have to read them
Something I keep coming back to: three years of appetite threads, summarised so you do not have to read them. 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. GIP…
Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.
Small fix — it slows gastric emptying, it does not halt it, and the distinction matters for the mechanism you are proposing.
Small fix — it slows gastric emptying, it does not halt it, and the distinction matters for the mechanism you are proposing.
This is the concept everything else on this board is downstream of.
That study was in a rodent model. Worth stating, since the thread has been reading it as human data.
gastric emptying slows, it does not stop
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.
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.
Does the effect persist with continued dosing or does tolerance develop?
Push back: a receptor being expressed in a tissue does not tell you the agonist reaches it at therapeutic exposure.
read the discussion section, that is where the honesty lives
read the discussion section, that is where the honesty lives
Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.
Tried to build a mental model from mechanism alone and produced a confident prediction that the trial data flatly contradicted.