Great question. The honest answer is: we're still figuring this out.
GIP receptors are expressed in the brain, including in the hypothalamus, and there's evidence that GIP signaling contributes to appetite regulation and may enhance the effects of GLP-1 receptor activation.1 Some researchers believe the dual agonism of tirzepatide explains its superior weight loss compared to semaglutide — it's hitting two complementary pathways.
However, the GIP receptor's role in the reward system is less well-characterized than GLP-1's. Most of the reward/food noise research has focused on GLP-1 specifically. It's an active area of investigation.
Anecdotally, many people on this forum report equal or greater food noise reduction on tirzepatide vs. semaglutide, which could support a GIP contribution. But anecdotes are not data, and we need more controlled studies.
The emerging triple agonists (GLP-1/GIP/glucagon, like retatrutide) will add another layer of complexity. Exciting times in this field.
1 Zhang et al., "GIP has neuroprotective effects in Alzheimer and Parkinson's disease models," Peptides, 2021.