AI Article Synopsis
- The study explored how immune responses, metabolism, and sleep are interconnected in mice with non-metastatic mammary cancer, focusing on the role of interleukin-6 (IL-6) and its effects.
- Tumor-bearing mice exhibited increased hunger, decreased leptin levels, and heightened sensitivity to ghrelin, with inflammation from IL-6 present but not entirely responsible for metabolic and sleep issues.
- By investigating specific brain neurons linked to metabolism and sleep, researchers found that blocking certain receptors improved metabolic health and sleep quality, highlighting the significance of neural signals in cancer-related metabolic changes.
Article Abstract
We investigated relationships among immune, metabolic, and sleep abnormalities in mice with non-metastatic mammary cancer. Tumor-bearing mice displayed interleukin-6 (IL-6)-mediated peripheral inflammation, coincident with altered hepatic glucose processing and sleep. Tumor-bearing mice were hyperphagic, had reduced serum leptin concentrations, and enhanced sensitivity to exogenous ghrelin. We tested whether these phenotypes were driven by inflammation using neutralizing monoclonal antibodies against IL-6; despite the reduction in IL-6 signaling, metabolic and sleep abnormalities persisted. We next investigated neural populations coupling metabolism and sleep, and observed altered activity within lateral-hypothalamic hypocretin/orexin (HO) neurons. We used a dual HO-receptor antagonist to test whether increased HO signaling was causing metabolic abnormalities. This approach rescued metabolic abnormalities and enhanced sleep quality in tumor-bearing mice. Peripheral sympathetic denervation prevented tumor-induced increases in serum glucose. Our results link metabolic and sleep abnormalities via the HO system, and provide evidence that central neuromodulators contribute to tumor-induced changes in metabolism.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031468 | PMC |
| http://dx.doi.org/10.1016/j.cmet.2018.04.021 | DOI Listing |
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