Kappa opioid receptor activation increases thermogenic energy expenditure which drives increased feeding.
Cell biology
Endocrinology
Neuroscience
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
21 Jul 2023
21 Jul 2023
Historique:
received:
17
01
2023
revised:
02
05
2023
accepted:
26
06
2023
medline:
24
7
2023
pubmed:
24
7
2023
entrez:
24
7
2023
Statut:
epublish
Résumé
Opioid receptors, including the kappa opioid receptor (KOR), exert control over thermoregulation and feeding behavior. Notably, activation of KOR stimulates food intake, leading to postulation that KOR signaling plays a central role in managing energy intake. KOR has also been proposed as a target for treating obesity. Herein, we report studies examining how roles for KOR signaling in regulating thermogenesis, feeding, and energy balance may be interrelated using pharmacological interventions, genetic tools, quantitative thermal imaging, and metabolic profiling. Our findings demonstrate that activation of KOR in the central nervous system causes increased energy expenditure via brown adipose tissue activation. Importantly, pharmacologic, or genetic inhibition of brown adipose tissue thermogenesis prevented the elevated food intake triggered by KOR activation. Furthermore, our data reveal that KOR-mediated thermogenesis elevation is reversibly disrupted by chronic high-fat diet, implicating KOR signaling as a potential mediator in high-fat diet-induced weight gain.
Identifiants
pubmed: 37485355
doi: 10.1016/j.isci.2023.107241
pii: S2589-0042(23)01318-4
pmc: PMC10362357
doi:
Types de publication
Journal Article
Langues
eng
Pagination
107241Subventions
Organisme : NIMH NIH HHS
ID : K08 MH119538
Pays : United States
Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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