A tachykinin-like neuroendocrine signalling axis couples central serotonin action and nutrient sensing with peripheral lipid metabolism

Lavinia Palamiuc, Tallie Noble, Emily Witham, Harkaranveer Ratanpal, Megan Vaughan and Supriya Srinivasan ()
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Lavinia Palamiuc: Department of Chemical Physiology and The Dorris Neuroscience Center
Tallie Noble: Mira Costa College
Emily Witham: The Scripps Research Institute
Harkaranveer Ratanpal: The Scripps Research Institute
Megan Vaughan: The Scripps Research Institute
Supriya Srinivasan: Department of Chemical Physiology and The Dorris Neuroscience Center

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract Serotonin, a central neuromodulator with ancient ties to feeding and metabolism, is a major driver of body fat loss. However, mechanisms by which central serotonin action leads to fat loss remain unknown. Here, we report that the FLP-7 neuropeptide and its cognate receptor, NPR-22, function as the ligand-receptor pair that defines the neuroendocrine axis of serotonergic body fat loss in Caenorhabditis elegans. FLP-7 is secreted as a neuroendocrine peptide in proportion to fluctuations in neural serotonin circuit functions, and its release is regulated from secretory neurons via the nutrient sensor AMPK. FLP-7 acts via the NPR-22/Tachykinin2 receptor in the intestine and drives fat loss via the adipocyte triglyceride lipase ATGL-1. Importantly, this ligand-receptor pair does not alter other serotonin-dependent behaviours including food intake. For global modulators such as serotonin, the use of distinct neuroendocrine peptides for each output may be one means to achieve phenotypic selectivity.

Date: 2017
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DOI: 10.1038/ncomms14237

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