{"title":"Brown fat fuels the fire in fever.","authors":"Samantha J Krysa, Jonathan R Brestoff","doi":"10.1016/j.jlr.2024.100658","DOIUrl":null,"url":null,"abstract":"<p><p>Fever is a host-pathogen defense mechanism in which the immune system drives a physiologic increase in core body temperature. For over 50 years, it has been known that the temperature of brown adipose tissue (BAT) is increased during the febrile response. However, recent studies suggested that the primary thermogenic protein Uncoupling protein 1 in brown adipocytes does not contribute to fever induction in mice, casting doubt about the functional contribution of BAT to fever. In a new set of studies, Li et al. (2024) provide compelling evidence that fatty acid oxidation is markedly increased in BAT in a Salmonella infection model of fever and strongly suggest that metabolic adaptation in BAT may play a critical role in the febrile response. This article re-opens the debate about how thermogenic and metabolic programs in BAT contribute to fever and raises new questions about whether BAT contributes to host defense against pathogens.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100658"},"PeriodicalIF":5.0000,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536056/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Lipid Research","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.jlr.2024.100658","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Fever is a host-pathogen defense mechanism in which the immune system drives a physiologic increase in core body temperature. For over 50 years, it has been known that the temperature of brown adipose tissue (BAT) is increased during the febrile response. However, recent studies suggested that the primary thermogenic protein Uncoupling protein 1 in brown adipocytes does not contribute to fever induction in mice, casting doubt about the functional contribution of BAT to fever. In a new set of studies, Li et al. (2024) provide compelling evidence that fatty acid oxidation is markedly increased in BAT in a Salmonella infection model of fever and strongly suggest that metabolic adaptation in BAT may play a critical role in the febrile response. This article re-opens the debate about how thermogenic and metabolic programs in BAT contribute to fever and raises new questions about whether BAT contributes to host defense against pathogens.
发热是一种宿主-病原体防御机制，在这种机制中，免疫系统促使核心体温生理性升高。50 多年来，人们一直知道发热反应期间棕色脂肪组织（BAT）温度会升高。然而，最近的研究表明，棕色脂肪细胞中的主要生热蛋白解偶联蛋白 1（UCP1）并不参与小鼠发热诱导，这使人们对棕色脂肪组织对发热的功能性贡献产生了怀疑。在一组新的研究中，Li 等人（2024 年）提供了令人信服的证据，证明在沙门氏菌感染发热模型中，BAT 中的脂肪酸氧化明显增加，并强烈建议 BAT 的代谢适应可能在发热反应中发挥关键作用。这篇文章再次引发了关于 BAT 产热和代谢程序如何导致发热的争论，并提出了关于 BAT 是否有助于宿主防御病原体的新问题。
期刊介绍：
The Journal of Lipid Research (JLR) publishes original articles and reviews in the broadly defined area of biological lipids. We encourage the submission of manuscripts relating to lipids, including those addressing problems in biochemistry, molecular biology, structural biology, cell biology, genetics, molecular medicine, clinical medicine and metabolism. Major criteria for acceptance of articles are new insights into mechanisms of lipid function and metabolism and/or genes regulating lipid metabolism along with sound primary experimental data. Interpretation of the data is the authors’ responsibility, and speculation should be labeled as such. Manuscripts that provide new ways of purifying, identifying and quantifying lipids are invited for the Methods section of the Journal. JLR encourages contributions from investigators in all countries, but articles must be submitted in clear and concise English.
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