GIP receptor agonism suppresses inflammation-induced aversion and food intake via distinct circuits.

ABSTRACT: Glucose-dependent insulinotropic polypeptide (GIP) is a gut-derived incretin hormone, and pharmacologic modulation of central GIP receptors (GIPR) improves energy homeostasis. Recent reports have demonstrated that GIPR agonism is also anti-aversive. However, the mechanisms by which GIPR signaling impact food intake and aversion are incompletely understood. Here, we show that GIPR agonism abrogates the aversive and enhances the anorexigenic effects of the pro-inflammatory cytokine interleukin-1β (IL-1β). Aversion-encoding parabrachial calcitonin-gene related peptide (CGRP) neurons were required for IL-1β-induced conditioned taste avoidance (CTA) but not anorexia. Moreover, systemic IL-1β increased in vivo CGRP neural activity, and this was significantly attenuated by co-administratio

SUBMITTER: Province HS 

PROVIDER: S-EPMC12363899 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature