mechanism — 21 things I got wrong before I got it right
Posting this as a discussion rather than a claim: mechanism — 21 things I got wrong before I got it right.
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.
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.
Happy to answer the boring questions. Those are usually the ones worth asking.
best — the order this archive was captured in
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.
gastric emptying slows, it does not stop
GIP is the arm people argue about because the biology is genuinely unsettled
Asked a question here that I thought was stupid and got three papers back. Best thread I have been in on this site.
Does the effect persist with continued dosing or does tolerance develop?
mechanism explains a direction, not a magnitude