Why appetite effects are mostly central

Why appetite effects are mostly central I have a specific reason for asking rather than idle curiosity, and the context is below.

Posting the method first, because I know what the first three replies will otherwise be.

• Column: C18, 4.6 x 250 mm, 5 um
• Mobile phase: 0.1% TFA in water / 0.1% TFA in acetonitrile
• Gradient: 10% to 53% organic over 19 minutes
• Detection: 280 nm
• Injection: 13 uL
• Sample: semaglutide, reconstituted to 1.0 mg/mL, injected within an hour

The main peak integrates at 96.4% of total area. There is a small feature on the trailing edge that I cannot decide is a shoulder or a baseline artefact, and that is what I am actually asking about.

Central versus peripheral action: GLP-1 agonism works through both central nervous system effects (appetite) and peripheral effects (gastric motility, insulin). The balance is not fully characterised.

I read the opening post twice before replying, because I had assumed the opposite.

Species differences: rodent studies show the same compounds produce effects in rodents that predict human effects reasonably well for semaglutide and tirzepatide. The track record is less clear for novel compounds with less human data.