On the subject in the title: Glucagon receptor agonism in a weight-loss compound Working notes rather than a conclusion.
Glucagon receptor agonism: setting out the arithmetic in full, because I have had to do it twice and I would rather nobody else did.
Every step is shown. If the answer is wrong the error will be visible, which is the point of writing it out rather than posting the result.
I had written a reply contradicting the opening post and deleted it. Here is what survived.
GIP receptor signalling: the glucose-dependent insulinotropic peptide receptor (GIP) is involved in glucose-stimulated insulin secretion. GIP agonism is thought to contribute to tirzepatide's effect but the mechanism is not fully settled.
That is one dataset and I would not build a rule on it.
Central versus peripheral action: GLP-1 agonism works through both central nervous system effects (appetite) and peripheral effects (gastric motility, insulin). The balance is not fully characterised.
Worth reading the earlier posts in this thread before acting on mine.
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