Hormonal
Systemic administration of the GIP receptor agonist DA-GIP suppresses inflammation-induced conditioned taste avoidance (CTA) and reduces parabrachial CGRP neuron activation, acting via distinct neural circuits than its anorectic effects.
For individuals experiencing severe nausea or food aversion due to inflammation (e.g., chronic autoimmune conditions or post-infection), standard anti-nausea medications (like ondansetron) or anti-inflammatories (NSAIDs) may not fully resolve the aversion. Emerging GIP-based therapies show promise in specifically targeting the neural circuits responsible for this aversion without necessarily worsening appetite suppression, potentially improving quality of life during inflammatory episodes.
GIPR agonism abrogates the aversive and enhances the anorexigenic effects of the pro-inflammatory cytokine interleukin-1β (IL-1β)... GIPR agonism reduces food intake and prevents aversion via distinct circuits
Why this rating
Preclinical mouse model study; high internal validity for mechanism but limited generalizability to humans without clinical trials.
Source
GIP receptor agonism suppresses inflammation-induced aversion and food intake via distinct circuits
Haley S. Province et al. · bioRxiv (Cold Spring Harbor Laboratory) · 2025
DOI 10.1101/2025.08.12.669936
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