Neuropeptides NLP-10 and FLP-18 stimulate lipid catabolism in chronically diet-restricted Caenorhabditis elegans
- 1Xiamen University
Abstract
Neuropeptides mediate inter-tissue communication in energy metabolism, yet most remain functionally uncharacterized. Using C. elegans, we uncover a neuropeptide signaling cascade that drives lipid catabolism under chronic dietary restriction. We show that impaired pharyngeal function leads to dyspepsia and nutrient insufficiency, which activates a signaling axis comprising two peptide-receptor pairs, NLP-10-NPR-35 and FLP-18-NPR-4. This cascade originates in ADL sensory neurons, relays through multiple interneurons, and enhances triglyceride hydrolysis in the intestine. Genetic disruption of any component of this axis restores fat accumulation in diet-restricted mutants, whereas overexpression of individual components in well-fed animals is insufficient to drive fat mobilization. Importantly, the same neuropeptide axis is engaged in starved wild-type animals, indicating a general response toward energy deficit rather than mutant-specific effects. These findings reveal a conserved neuroendocrine circuit that senses internal energy shortage and orchestrates systemic metabolic adaptation, providing a conceptual framework for how neuropeptide networks integrate nutritional status with energy balance in animals.
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BibTeX
@misc{liu2026neuropeptides,
title = {{Neuropeptides NLP-10 and FLP-18 stimulate lipid catabolism in chronically diet-restricted Caenorhabditis elegans}},
author = {J. Liu and L. Lin and L. Yao and Y. Yu and J. Luo},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.17.752367},
url = {https://www.biorxiv.org/content/10.64898/2026.09.17.752367v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Neuropeptides NLP-10 and FLP-18 stimulate lipid catabolism in chronically diet-restricted Caenorhabditis elegans
AU - J. Liu
AU - L. Lin
AU - L. Yao
AU - Y. Yu
AU - J. Luo
PY - 2026
DA - 2026/09/17
PB - bioRxiv
DO - 10.64898/2026.09.17.752367
UR - https://www.biorxiv.org/content/10.64898/2026.09.17.752367v1
AB - Neuropeptides mediate inter-tissue communication in energy metabolism, yet most remain functionally uncharacterized. Using C. elegans, we uncover a neuropeptide signaling cascade that drives lipid catabolism under chronic dietary restriction. We show that impaired pharyngeal function leads to dyspepsia and nutrient insufficiency, which activates a signaling axis comprising two peptide-receptor pairs, NLP-10-NPR-35 and FLP-18-NPR-4. This cascade originates in ADL sensory neurons, relays through multiple interneurons, and enhances triglyceride hydrolysis in the intestine. Genetic disruption of any component of this axis restores fat accumulation in diet-restricted mutants, whereas overexpression of individual components in well-fed animals is insufficient to drive fat mobilization. Importantly, the same neuropeptide axis is engaged in starved wild-type animals, indicating a general response toward energy deficit rather than mutant-specific effects. These findings reveal a conserved neuroendocrine circuit that senses internal energy shortage and orchestrates systemic metabolic adaptation, providing a conceptual framework for how neuropeptide networks integrate nutritional status with energy balance in animals.
ER -