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c/glp1science·posted 2 years ago by u/maintenance_mode_max

genuine question about receptor that I am slightly embarrassed to ask

Needs Source Receipts ×6 Cold Box ×1 Well Actually ×2

Posting this because I searched for it and got nothing useful.

Setup: 10mg, week 27, constipation present but not ruining anything. I changed exactly one variable — receptor — and tracked it for 10 weeks.

Result: a difference, but a small one, and well inside what I would call noise if someone else posted it. So I am putting it here rather than presenting it as a finding. If two or three other people have done the same thing we might actually learn something.

Not medical advice, obviously. This is one person with a spreadsheet.

3,872 up / 277 down93% upvoted27 commentsid 1y9l6n17 Apr 2024

27 comments

24 in this archive, depth 4

best — the order this archive was captured in

u/signe_boateng428 points·2 years ago

I am going to push back on this slightly.

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u/cato_batista181 points·2 years ago

receptor distribution matters, GLP-1 is not everywhere

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u/gastric_emptying_g346 points·2 years ago

Yeah, the incretin mechanism is doing the work here.

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u/viktor_girard93 points·2 years ago

Which paper are you quoting?

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u/farid_kuipers40 points·2 years ago

rodent gastric emptying tells you what to investigate, not what to expect in humans

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u/trialwatch_theoMOD176 points·2 years ago

Removed a chain here. The rule is one line long and it is not negotiable.

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u/niels_roos178 points·2 years ago·edited

Is that mechanism or speculation?

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u/anya_salgado141 points·2 years ago

cite the paper: journal, year, first author, links optional

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u/tomas_lundgren109 points·2 years ago·edited

Yeah, the incretin mechanism is doing the work here.

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u/devils_advocate_d150 points·2 years ago

central appetite signalling is real but people overweight it

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u/amara_dziedzic79 points·2 years ago

gastric emptying is real and explains most early the food-noise thing

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u/bastian_eriksen75 points·2 years ago

Is that mechanism or speculation?

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u/ismael_eriksen48 points·2 years ago·edited

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

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u/noor_hovland38 points·2 years ago·edited

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

Adding to this: half-life is doing more work than the comment implies.

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u/gustav_vermeulen21 points·2 years ago·edited

receptor distribution matters, GLP-1 is not everywhere

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u/nora_lundgren61 points·2 years ago

Slight fix: the number was 99.1, not 99.0. Decimal point, but a fairly consequential one.

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u/maintenance_mode_maxOPmaintenance37 points·2 years ago

glucagon-receptor contribution is incretin for dual and triple agonism

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u/asks_dumb_questions83 points·2 years ago

Yeah, the incretin mechanism is doing the work here.

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u/incretin_ivypharmacology51 points·2 years ago

Stomach physiology changed when I moved up to 12.5mg. Gastric emptying lag is the whole story.

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u/yusuf_ramos55 points·2 years ago

do not extrapolate rodent data to human dosing without saying so

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u/bilal_osei44 points·2 years ago

receptor distribution matters, GLP-1 is not everywhere

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About c/glp1science

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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