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c/glp1science·submitted 7 days ago by u/sig_figs_sam

[Paper] receptor distribution and why the GI effects were predictable

Paperbranch of 7 comments

receptor distribution and why the GI effects were predictable. Change my mind, genuinely — I have no stake in being right about this. Tried to build a mental model from mechanism alone and produced a confident prediction that the trial data flatly contradicted. Spent an evening on the receptor distribution literature…

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7 comments, started 6 days ago
u/incretin_ivyMOD16 points·6 days ago

Retitled to distinguish preclinical from clinical, which the original ran together.

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u/rina_bergstrom13 points·6 days ago

the peripheral and central stories are not in competition

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[removed]9 points·5 days ago

[removed by moderator]

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u/osman_eriksen9 points·5 days ago

Read the primary paper after arguing about the summary for a fortnight. The discussion section said almost the opposite of what the thread had concluded.

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u/gradient_goblin6 points·5 days ago

Correction: that is glucose-dependent insulin secretion, which is why hypoglycaemia risk is low as monotherapy. Not the same claim as you made.

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u/plain_titration9 points·6 days ago

Retitled to distinguish preclinical from clinical, which the original ran together.

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

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u/sig_figs_samOPmod · analytical4 points·6 days ago

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

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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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