Caffeine inhibits hypothalamic A1R to excite oxytocin neuron and ameliorate dietary obesity in mice

Liufeng Wu, Jia Meng, Qing Shen, Yi Zhang, Susu Pan, Zhuo Chen, Ling-Qiang Zhu, Youming Lu, Yuan Huang and Guo Zhang ()
Additional contact information
Liufeng Wu: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Jia Meng: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Qing Shen: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Yi Zhang: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Susu Pan: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Zhuo Chen: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Ling-Qiang Zhu: Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology
Youming Lu: Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology
Yuan Huang: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology
Guo Zhang: Key Laboratory of Environmental Health, Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Caffeine, an antagonist of the adenosine receptor A1R, is used as a dietary supplement to reduce body weight, although the underlying mechanism is unclear. Here, we report that adenosine level in the cerebrospinal fluid, and hypothalamic expression of A1R, are increased in the diet-induced obesity (DIO) mouse. We find that mice with overexpression of A1R in the neurons of paraventricular nucleus (PVN) of the hypothalamus are hyperphagic, have glucose intolerance and high body weight. Central or peripheral administration of caffeine reduces the body weight of DIO mice by the suppression of appetite and increasing of energy expenditure. We also show that caffeine excites oxytocin expressing neurons, and blockade of the action of oxytocin significantly attenuates the effect of caffeine on energy balance. These data suggest that caffeine inhibits A1Rs expressed on PVN oxytocin neurons to negatively regulate energy balance in DIO mice.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms15904 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15904

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms15904

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().