期刊
CELL REPORTS
卷 19, 期 2, 页码 267-280出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.03.043
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资金
- Deutsche Forschungsgemeinschaft (DFG) [BR 1492/7-1]
- DFG [TRR134]
- German Federal and State Governments (CECAD)
- Helmholtz Alliance ICEMED Imaging and Curing Environmental Metabolic Diseases, through the Initiative and Networking Fund of the Helmholtz Association
- European Union [266408]
- Advanced Postdoc Grant from the Swiss National Science Foundation
- Early Career Research Grant from the University of Basel, Switzerland
Interleukin (IL)-6 engages similar signaling mechanisms to leptin. Here, we find that central application of IL-6 in mice suppresses feeding and improves glucose tolerance. In contrast to leptin, whose action is attenuated in obesity, the ability of IL-6 to suppress feeding is enhanced in obese mice. IL-6 suppresses feeding in the absence of neuronal IL-6-receptor (IL-6R) expression in hypothalamic or all forebrain neurons of mice. Conversely, obese mice exhibit increased soluble IL-6R levels in the cerebrospinal fluid. Blocking IL-6 trans-signaling in the CNS abrogates the ability of IL-6 to suppress feeding. Furthermore, gp130 expression is enhanced in the paraventricular nucleus of the hypothalamus (PVH) of obese mice, and deletion of gp130 in the PVH attenuates the beneficial central IL-6 effects on metabolism. Collectively, these experiments indicate that IL-6 trans-signaling is enhanced in the CNS of obese mice, allowing IL-6 to exert its beneficial metabolic effects even under conditions of leptin resistance.
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