Author
Listed:
- 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
School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology)
- Youming Lu
(Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology
School of Basic Medicine, Tongji Medical College, 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
Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology)
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.
Suggested Citation
Liufeng Wu & Jia Meng & Qing Shen & Yi Zhang & Susu Pan & Zhuo Chen & Ling-Qiang Zhu & Youming Lu & Yuan Huang & Guo Zhang, 2017.
"Caffeine inhibits hypothalamic A1R to excite oxytocin neuron and ameliorate dietary obesity in mice,"
Nature Communications, Nature, vol. 8(1), pages 1-15, August.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15904
DOI: 10.1038/ncomms15904
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