Une publication essentielle pour mieux comprendre la perte de poins adrénaline et serotonine sont impliquées, celà n'est pas nouveau ce qui l'est c'est l'identification d'un signal spécifique chez le ver.
An Integrated Serotonin and Octopamine Neuronal Circuit Directs the Release of an Endocrine Signal to ControlC. elegans Body Fat
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Cell Metabolism, 10 October 2013
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.cmet.2013.09.007
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.cmet.2013.09.007
Authors
- Highlights
- Integrated 5-HT and Oct signaling from neurons synergize to stimulate body fat loss
- Oct, an analog of adrenaline, acts as a permissive cue to maintain 5-HT signaling
- A 5-HTergic channel relays an instructive endocrine signal via body cavity neurons
- The endocrine signal is relayed to the intestinal lipase ATGL to induce fat loss
Summary
Serotonin (5-hydroxytryptamine, 5-HT) is an ancient and conserved neuromodulator of energy balance. Despite its importance, the neural circuits and molecular mechanisms underlying 5-HT-mediated control of body fat remain poorly understood. Here, we decipher the serotonergic neural circuit for body fat loss in C. elegans and show that the effects of 5-HT require signaling from octopamine, the invertebrate analog of adrenaline, to sustain body fat loss. Our results provide a potential molecular explanation for the long-observed potent effects of combined serotonergic and adrenergic weight loss drugs. In metabolic tissues, we find that the conserved regulatory adipocyte triglyceride lipase ATGL-1 drives serotonergic fat loss. We show that the serotonergic chloride channel MOD-1 relays a long-range endocrine signal from C. elegans body cavity neurons to control distal ATGL-1 function, via the nuclear receptor NHR-76. Our findings establish a conserved neuroendocrine axis operated by neural serotonergic and adrenergic-like signaling to regulate body fat.
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