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c/glp1science·submitted 1 year ago by u/bastian_ekstrom

three years of mechanism threads, summarised so you do not have to read them

Questionbranch of 6 comments

three years of mechanism threads, summarised so you do not have to read them, and I am aware this is a minority view on this board. 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…

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6 comments, started 1 year ago
u/trialwatch_theoMOD257 points·1 year ago

Left up and flaired Explainer. This is the standard of post the board was created for.

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u/ilias_kaufmann104 points·1 year ago

Agreed that receptor distribution is the key to the side-effect map. It is not a mystery, it is anatomy.

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u/bastian_ekstromOP52 points·1 year 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/saskia_lokken58 points·1 year ago

Asked a question here that I thought was stupid and got three papers back. Best thread I have been in on this site.

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u/split_dose_sceptic62 points·1 year ago

What does the discussion section say about the limitation you are glossing?

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u/nadia_bakker27 points·1 year ago

The incretin effect is the observation that oral glucose provokes a larger insulin response than intravenous glucose at matched glycaemia, and the difference is mediated by gut hormones. That is the foundation the whole class sits on.

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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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