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Single comment threadYou are looking at one branch of the mechanism question that gets asked weekly, answered properly — 19 comments in the full submission. View in context.
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c/glp1science·submitted 2 years ago by u/santiago_rasmussen

the mechanism question that gets asked weekly, answered properly

Paperbranch of 12 comments

the mechanism question that gets asked weekly, answered properly. 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…

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12 comments, started 2 years ago
u/nora_lundgren40 points·2 years 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/gastric_emptying_gMOD23 points·2 years ago

Asked for a citation rather than removing. On this board a claim without one is an invitation, not an offence.

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u/incretin_ivypharmacology-22 points·2 years ago

receptor agonism is not the same as receptor activation in every tissue

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u/whois_wanda5 points·2 years ago

glucagon agonism sounds paradoxical until you read the energy expenditure work

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u/santiago_rasmussenOP3 points·2 years ago

Does the effect persist with continued dosing or does tolerance develop?

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u/mod_ambulatoryadmin2 points·2 years ago

Disagree. That is a preclinical finding in a rodent model and you are stating it as human pharmacology.

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u/santiago_rasmussenOP2 points·2 years ago

That study was in a rodent model. Worth stating, since the thread has been reading it as human data.

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u/greta_lokken2 points·2 years ago

read the discussion section, that is where the honesty lives

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u/priya_guerrero27 points·2 years 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/laila_almeida19 points·2 years ago

Small fix — it slows gastric emptying, it does not halt it, and the distinction matters for the mechanism you are proposing.

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u/split_dose_sceptic10 points·2 years ago

The mental model, in four steps, that makes the rest of this site legible.

One: gut hormones amplify the insulin response to food. Two: agonists at those receptors act peripherally on insulin secretion and gastric emptying, and centrally on appetite. Three: structural modification gives them a long half-life, so exposure is smooth and weekly. Four: tolerance develops to some effects and not to others.

From those four, most of what the experience boards report falls out: why the side effects cluster early, why they settle at a stable dose, why appetite reduction persists, and why the scale and the appetite move on different clocks.

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u/dose_creep_dan3 points·2 years ago

dose response is not linear and nobody should assume it is

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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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