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Blunted Vagal Cocaine- and Amphetamine-Regulated Transcript Promotes Hyperphagia and Weight Gain

Journal article
Authors S. J. Lee
Jean-Philippe Krieger
M. Vergara
D. Quinn
M. McDougle
A. de Araujo
R. Darling
B. Zollinger
S. Anderson
A. Pan
E. J. Simonnet
A. Pignalosa
M. Arnold
A. Singh
W. Langhans
H. E. Raybould
G. de Lartigue
Published in Cell Reports
Volume 30
Issue 6
Pages 2028-2039.e4
ISSN 2211-1247
Publication year 2020
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 2028-2039.e4
Language en
Links dx.doi.org/10.1016/j.celrep.2020.01...
Keywords afferent neurons, glp-1 receptors, sensory neurons, cart peptides, reduces food, fatty-acids, c-fos, cholecystokinin, obesity, expression, Cell Biology
Subject categories Physiology, Cell biology

Abstract

The vagus nerve conveys gastrointestinal cues to the brain to control eating behavior. In obesity, vagally mediated gut-brain signaling is disrupted. Here, we show that the cocaine- and amphetamine-regulated transcript (CART) is a neuropeptide synthesized proportional to the food consumed in vagal afferent neurons (VANs) of chow-fed rats. CART injection into the nucleus tractus solitarii (NTS), the site of vagal afferent central termination, reduces food intake. Conversely, blocking endogenous CART action in the NTS increases food intake in chow-fed rats, and this requires intact VANs. Viral-mediated Cartpt knockdown in VANs increases weight gain and daily food intake via larger meals and faster ingestion rate. In obese rats fed a high-fat, high-sugar diet, meal-induced CART synthesis in VANs is blunted and CART antibody fails to increase food intake. However, CART injection into the NTS retains its anorexigenic effect in obese rats. Restoring disrupted VAN CART signaling in obesity could be a promising therapeutic approach.

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