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c/glp1science·submitted 3 months ago by u/ireland_drugs_pay

[Question] how do you actually verify pharmacology

Questionbranch of 7 comments

how do you actually verify pharmacology. I would rather ask a basic question now than get this wrong quietly for two months. 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…

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7 comments, started 3 months ago
u/formulary_fighterappeals107 points·3 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/analog_alphabet51 points·3 months ago·edited

Same view.

Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.

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u/vikram_mbeki40 points·3 months ago

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

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u/niels_roos14 points·3 months ago

Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.

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

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u/lina_ndiaye29 points·3 months ago

Right — mechanism gives you a direction. It never gives you an effect size and people use it as though it does.

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u/tomas_lundgren7 points·3 months ago

The half-life explanation was the thing that made weekly dosing intuitive for me rather than arbitrary.

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u/ingrid_correia14 points·3 months ago

Cosigning on GIP. The genuinely interesting thing is that the biology is not settled and the clinical result is nonetheless robust.

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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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