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c/glp1science·submitted 18 days ago by u/aleksi_eriksen

[Paper] amylin co-agonism is genuinely different pharmacology, not just more GLP-1

Paperbranch of 9 comments

Long-ish post, sorry. tl;dr at the bottom. I have been tracking incretin against triglycerides for 13 weeks because I could not find anyone who had. The correlation is weaker than I expected, which is itself mildly interesting given how confidently people link the two in here. Caveats up front: one person, one lab,…

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9 comments, started 16 days ago
u/gustav_vermeulen29 points·16 days ago
i have this exact spreadsheet
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u/yannick_barros18 points·16 days ago

Yeah, the incretin mechanism is doing the work here.

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u/gustav_vermeulen7 points·15 days ago

Strongly agree. Central appetite is real but people overstate it.

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u/rohan_steiner2 points·15 days ago

gastric emptying is real and explains most early early fullness

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u/aleksi_eriksenOP17 points·16 days ago

glucagon-receptor contribution is appetite for dual and triple agonism

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u/camila_mensa16 points·15 days ago

This is correct. Rodent data is investigational, not predictive.

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u/annika_fonseca9 points·15 days ago

This is the "correlation is mechanism" thing again. You changed three variables at once.

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u/milan_mensah5 points·15 days ago

glucagon-receptor contribution is gastric emptying for dual and triple agonism

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u/rohan_steiner1 point·15 days ago

amylin is not GLP-1, posts conflating them get corrected

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