Topic summary

Amylin receptor signalling and satiety — what changed since

Pharmacology › Receptor biology tirzepatide retatrutide long read amylin analogues

This is a generated summary. It shows the 9 most-liked posts from a topic of 79, in their original order, with the accepted answer included where one exists. It is a reading aid and it will miss nuance — the full topic is the record.

glossary_checkTL2Member30 Nov 2025#1

On the subject in the title: Amylin receptor signalling and satiety — what changed since Working notes rather than a conclusion.

What changes if the standard account of Amylin receptor signalling and satiety is wrong? I ask because I have been treating it as settled and I noticed this week that I could not say why.

Working through the consequences rather than the evidence, since others here are better placed on the evidence.

48 likes 8mo

s.bergstromTL230 Jan 2026#23

Agreed on all of that, and I have nothing to add to it.

30 likes 6mo

sa.vogelTL28 Feb 2026#27

Amylin receptor signalling: amylin promotes satiety and slows gastric emptying through a receptor distinct from GLP-1. The hypothesis behind combination therapy is two complementary satiety mechanisms.

22 likes 6mo

y.adeyemiTL26 Mar 2026 · edited#40

Post #37 is the version of this I will quote in future. One addition.

The area postrema sits outside the blood-brain barrier and is where a great deal of the nausea signalling in this class originates. That is why the effect is central and not gastric irritation.

29 likes 5mo

sterile_fileTL3Regular19 Mar 2026#47

y.ramos, post #42: Mechanistic plausibility has a poor record of predicting clinical outcomes across this whole field. It is a good reason to run the trial and a bad reason to skip it. Go to post

Glucagon receptor agonism raises energy expenditure and promotes hepatic fat oxidation. In a triple agonist the incretin limbs offset the glycaemic consequence, which is why the combination is not self-defeating.

26 likes in reply to #42 4mo

NorringtonTL3Regular28 Mar 2026#52

Tavares, post #6: Reading back through, this was answered upthread and I missed it. My fault. Go to post

Post #49 is the version of this I will quote in future. One addition.

Receptor occupancy required for a clinical effect is not the same as full occupancy, and dose-response curves flattening at the top is what you would expect from that.

26 likes in reply to #6 4mo

h.agyemanTL215 Apr 2026#62

Reporting rather than recommending, on Amylin receptor signalling and satiety. What happened is above. Whether it should have is a different question and not one I am qualified to answer.

23 likes 3mo

n.cabreraTL222 Apr 2026#66

Ghrelin receptor agonism drives growth hormone release in pulses and also increases appetite, which is the effect people most reliably report and least often want.

Not disagreeing with anyone above, just adding the bit I keep having to look up.

31 likes 3mo

b.aaltoTL227 Apr 2026#69

cannula_drift, post #28: Pharmacological class effects: all GLP-1 agonists slow gastric emptying and suppress appetite. Those are class effects, not unique to one compound. Effects that differ between compounds are usually about potency or receptor selectivity. Go to post

Receptor desensitisation and internalisation are real phenomena in vitro and their clinical relevance to these compounds is not established. That distinction gets lost in discussions about tolerance.

22 likes in reply to #28 3mo

Read the full topic (79 posts)

Moved from Pharmacokinetics by s.leclerc. Category placement is not obvious from outside and getting it wrong is expected. This topic will get better answers here. The move is recorded in the public log citing R7.

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