Journal article
Opioidergic signaling contributes to food-mediated suppression of AgRP neurons
Cell reports (Cambridge), Vol.43(1), 113630
01/01/2024
DOI: 10.1016/j.celrep.2023.113630
PMCID: PMC10865729
PMID: 38165803
Abstract
Opioids are generally known to promote hedonic food consumption. Although much of the existing evidence is primarily based on studies of the mesolimbic pathway, endogenous opioids and their receptors are widely expressed in hypothalamic appetite circuits as well; however, their role in homeostatic feeding remains unclear. Using a fluorescent opioid sensor, deltaLight, here we report that mediobasal hypothalamic opioid levels increase by feeding, which directly and indirectly inhibits agouti-related protein (AgRP)-expressing neurons through the μ-opioid receptor (MOR). AgRP-specific MOR expression increases by energy surfeit and contributes to opioid-induced suppression of appetite. Conversely, its antagonists diminish suppression of AgRP neuron activity by food and satiety hormones. Mice with AgRP neuron-specific ablation of MOR expression have increased fat preference without increased motivation. These results suggest that post-ingestion release of endogenous opioids contributes to AgRP neuron inhibition to shape food choice through MOR signaling.
Details
- Title: Subtitle
- Opioidergic signaling contributes to food-mediated suppression of AgRP neurons
- Creators
- Nilufer Sayar-Atasoy - Department of Neuroscience and Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USAYavuz Yavuz - Yeditepe UniversityConnor Laule - University of IowaChunyang Dong - University of California, DavisHyojin Kim - University of IowaJacob Rysted - University of IowaKyle Flippo - University of IowaDebbie Davis - Department of Neuroscience and Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USAIltan Aklan - University of IowaBayram Yilmaz - Yeditepe UniversityLin Tian - University of California, DavisDeniz Atasoy - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Cell reports (Cambridge), Vol.43(1), 113630
- DOI
- 10.1016/j.celrep.2023.113630
- PMID
- 38165803
- PMCID
- PMC10865729
- NLM abbreviation
- Cell Rep
- ISSN
- 2211-1247
- eISSN
- 2211-1247
- Grant note
- R01 DK126740 / NIDDK NIH HHS
- Language
- English
- Date published
- 01/01/2024
- Academic Unit
- Neurology; Pathology; Iowa Neuroscience Institute; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984539532202771
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