Hormonal
Leptin signaling via hypothalamic LepRbGlp1r neurons is the primary driver of food intake suppression, as ablating this receptor causes hyperphagic obesity without impairing energy expenditure.
This research identifies a specific brain pathway (LepRbGlp1r neurons) that leptin uses to tell you to stop eating. When this pathway is broken or ignored, you eat more regardless of how much energy you burn. This explains why some obesity treatments focus on mimicking these signals (like GLP-1 drugs) to restore the 'stop eating' signal rather than just forcing exercise.
Ablating Lepr from LepRbGlp1r cells provoked hyperphagic obesity without impairing energy expenditure.
Why this rating
High-fidelity genetic manipulation (knockout/reactivation) in mouse models with clear phenotypic outcomes.
Source
Suppression of food intake by Glp1r/Lepr-coexpressing neurons prevents obesity in mouse models
Alan C. Rupp et al. · Journal of Clinical Investigation · 2023
DOI 10.1172/jci157515
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