pharmacology is the most under-discussed thing on this board
pharmacology is the most under-discussed thing on this board. Change my mind, genuinely — I have no stake in being right about this.
GIP receptor biology is genuinely unsettled — there is a live argument about agonism versus antagonism at the receptor — and the clinical results are robust regardless, which is an uncomfortable and interesting position.
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.
Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.
If two or three other people have done the same thing we might actually learn something. Alone it is an anecdote.
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.
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.
Was completely wrong about the gastric emptying story in a thread here two years ago.
Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.
Is that from a human study or a preclinical model?
Disagree. That is a preclinical finding in a rodent model and you are stating it as human pharmacology.
Disagree.
Agreed — and it is why the central and peripheral stories are complementary rather than rival.
GLP-1 receptor agonism acts both peripherally — insulin secretion in a glucose-dependent way, slowed gastric emptying — and centrally, on appetite regulation. The central component is the better explanation for sustained intake reduction.