Caffeine inhibits hypothalamic A1R to excite oxytocin neuron and ameliorate dietary obesity in mice
Wu L, Meng J, Shen Q, Zhang Y, Pan S, Chen Z, Zhu LQ, Lu Y, Huang Y, Zhang G
Nature communications · 67 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Government
- National Natural Science Foundation of China
- University or hospital
- Huazhong University of Science and Technology
- Government
- Natural Science Foundation of Hubei Province
- Government
- Recruitment Program of Global Experts
- Grants
- National Natural Science Foundation of China (81573146); National Natural Science Foundation of China (91539125)
Based on 4 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2017-06-27 · Nat Commun · vol. 8 · issue 1 · p. 15904
- Publisher
- Nature Portfolio
- Cited
- 80 citations · more than 89% of similar papers · 2.5× the field average
- References
- 71 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Regulation of Appetite and Obesity · Eating Disorders and Behaviors · Pancreatic function and diabetes
- Keywords
- Caffeine, Oxytocin, Endocrinology, Internal medicine, Hypothalamus, Adenosine, Diet-induced obese, Appetite, Antagonist, Medicine, Obesity, Oxytocin receptor, Blockade, Neuron, Receptor, Chemistry, Biology, Neuroscience, Insulin resistance
- MeSH
- hypothalamus, paraventricular hypothalamic nucleus, neurons, animals, mice, inbred c57bl, humans, mice, obesity, caffeine, leptin, oxytocin, glucose, receptors, purinergic p1, energy metabolism, male, purinergic p1 receptor antagonists, diet, high-fat
10 authors
From CN
- Liufeng WuHuazhong University of Science and Technology
- Meng JiaHuazhong University of Science and Technology
- Qing Xiang ShenHuazhong University of Science and Technology
- Yi ZhangHuazhong University of Science and Technology
- Susu PanHuazhong University of Science and Technology
- Zhuo ChenHuazhong 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.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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