ArticleCell reports2026
FGF21 signals through hindbrain neurons to alter food intake and energy expenditure during dietary protein restriction.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The hallmarks of protein and amino acid restriction in aging and longevity.Cell press blue · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
The metabolic hormone fibroblast growth factor 21 (FGF21) is essential for adaptive responses to dietary protein restriction, but the precise neural circuit mediating these effects remains undefined. Here, we demonstrate that a discrete population of glutamatergic, Klb-expressing neurons in the nucleus of the solitary tract (NTS) mediates FGF21 action during protein restriction. Using a Klb-Flp mouse line combined with intersectional genetics, we show that NTS-beta-klotho (KLB) neurons are directly activated by FGF21. Systematic evaluation of previously implicated regions (suprachiasmatic nucleus [SCN], paraventricular nucleus [PVN], and ventromedial hypothalamus [VMH]) reveals these areas are not required for FGF21-mediated responses to protein restriction. In contrast, selective ablation of NTS-KLB neurons prevents metabolic adaptations to protein restriction, including changes in food intake, food choice, and energy expenditure, while their chemogenetic activation is sufficient to drive these responses. These findings establish that NTS-KLB neurons directly respond to FGF21 and coordinate adaptive changes during protein restriction, identifying the neural circuit linking dietary protein sensing to metabolic adaptation.
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Registered trials
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