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c/glp1science·submitted 10 months ago by u/incretin_ivy

why does nobody talk about mechanism

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why does nobody talk about mechanism, and I want the answer with the reasoning attached rather than just the conclusion. 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…

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7 comments, started 10 months ago
u/elodie_grimaldi87 points·10 months ago

Same view. Tolerance developing to the gastric effect while the appetite effect persists explains most of what the side-effect board reports.

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u/bastian_eriksen43 points·10 months ago

Not convinced by the linearity assumption. Dose-response in this class is not linear and the trials show it.

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u/trialwatch_theotrial nerd10 points·10 months ago

incretin effect first, then everything else in this board makes sense

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u/camila_mensa66 points·10 months ago

Started reading limitations sections first. It has changed how much weight I give to almost everything posted here.

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u/ingrid_correia17 points·10 months ago

Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.

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u/dose_creep_dan4 points·10 months ago

Went looking for human data on a mechanism everybody here asserts. Found preclinical work and one small study. That was clarifying.

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u/devils_advocate_d2 points·10 months ago

Went looking for human data on a mechanism everybody here asserts.

Agreed — and it is why the central and peripheral stories are complementary rather than rival.

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The mechanism layer: incretin physiology, receptor distribution, gastric emptying, central appetite signalling, glucagon-receptor contribution, amylin co-agonism, and the pharmacokinetics that make weekly dosing possible. Papers get cited by journal and year or they get a [needs source] reply.

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