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Hedonic eating is controlled by dopamine neurons that oppose GLP-1R satiety.

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Science. 2025 Mar 28;387(6741):eadt0773. doi: 10.1126/science.adt0773
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Hedonic eating is controlled by dopamine neurons that oppose GLP-1R satiety.
Zhu Z, Gong R, Rodriguez V, Quach KT, Chen X, Sternson SM
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Abstract

Hedonic eating is defined as food consumption driven by palatability without physiological need. However, neural control of palatable food intake is poorly understood. We discovered that hedonic eating is controlled by a neural pathway from the peri-locus ceruleus to the ventral tegmental area (VTA). Using photometry-calibrated optogenetics, we found that VTA dopamine (VTA) neurons encode palatability to bidirectionally regulate hedonic food consumption. VTA neuron responsiveness was suppressed during food consumption by semaglutide, a glucagon-like peptide receptor 1 (GLP-1R) agonist used as an antiobesity drug. Mice recovered palatable food appetite and VTA neuron activity during repeated semaglutide treatment, which was reversed by consumption-triggered VTA neuron inhibition. Thus, hedonic food intake activates VTA neurons, which sustain further consumption, a mechanism that opposes appetite reduction by semaglutide.

PMID: 40146831 [PubMed - indexed for MEDLINE]

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Janelia Authors

Rong Gong
Scott Sternson
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