Hormonal
GIP receptor (GIPR) agonism suppresses inflammation-induced conditioned taste avoidance (aversion) by attenuating the activity of parabrachial CGRP neurons, while simultaneously enhancing inflammation-induced anorexia via distinct dorsal vagal complex (DVC) circuits.
If you are experiencing sickness-induced nausea and loss of appetite, standard anti-nausea drugs might not stop the feeling of aversion, and standard anti-inflammatories might not stop the nausea. This research suggests that GIP-based therapies could specifically target the 'sickness feeling' (aversion) via brain circuits, potentially allowing patients to feel better without necessarily worsening their lack of appetite, though it does increase food suppression. This is currently experimental in mice.
Here, we show that GIPR agonism abrogates the aversive and enhances the anorexigenic effects of the pro-inflammatory cytokine interleukin-1β (IL-1β)... Taken together, our data suggest that GIPR agonism reduces food intake and prevents aversion via distinct circuits.
Why this rating
The study is a preprint (bioRxiv) and uses murine models, limiting direct human applicability and peer-review status.
Source
GIP receptor agonism suppresses inflammation-induced aversion and food intake via distinct circuits
Haley S. Province et al. · Cell Reports · 2026
DOI 10.1016/j.celrep.2026.117116
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