ArticleCell reports2025
Sensory-neuron-derived CGRPα controls white adipocyte differentiation and tissue plasticity.
Article in Cell reports, 2025. 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
25 authors.
Funding
Abstract
Communication between the brain and adipose tissue is mediated in part by the peripheral nervous system. The sympathetic branch transmits lipolytic and thermogenic signals toward adipose tissue, while sensory nerves relay information to the central nervous system. Importantly, sensory nerve activation also triggers local neuropeptide release. Here, we show that sensory-neuron-derived α-calcitonin gene-related peptide (CGRPα) inhibits white, but not brown, preadipocyte differentiation in a cell-autonomous manner. In vivo, CGRPα expression in mouse subcutaneous adipose tissue during cold exposure shifts the expected increase in smaller adipocytes to an increase in larger cells. Importantly, people on anti-CGRPα/CGRP receptor (CGRPR) medications for migraine treatment show reductions in weight and glycemia, while these measures increase in the matched control group. Similarly, mice treated with a CGRPR antagonist and exposed to cold show a reduction in body weight. These findings identify a neuron-adipocyte communication pathway that regulates white adipose tissue plasticity and metabolism.
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