Adipose Tissue-Resident Sphingomonas Paucimobilis Suppresses Adaptive Thermogenesis by Reducing 15-HETE Production and Inhibiting AMPK Pathway
文献类型： 外文期刊
作者： Zhu, Yucheng 1 ; Yang, Ruiqi 1 ; Deng, Zhangchao 1 ; Deng, Bohua 1 ; Zhao, Kun 2 ; Dai, Chen 3 ; Wei, Gang 4 ; Wang, Yanjiang 5 ; Zheng, Jinshui 6 ; Ren, Zhuqing 1 ; Lv, Wentao 7 ; Xiao, Yingping 7 ; Mei, Zhinan 8 ; Song, Tongxing 1 ;
作者机构： 1.Huazhong Agr Univ, Coll Anim Sci & Technol, Wuhan 430070, Peoples R China
2.Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Endocrinol, Beijing 100700, Peoples R China
3.Huazhong Univ Sci & Technol, Tongji Hosp, Inst Organ Transplantat, Tongji Med Coll, Wuhan 430030, Peoples R China
4.Capital Med Univ, Beijing Tongren Hosp, Beijing Diabet Inst, Beijing Key Lab Diabet Res & Care,Dept Endocrinol, Beijing 100730, Peoples R China
5.Capital Med Univ, Beijing Chao Yang Hosp, Beijing 100020, Peoples R China
6.Huazhong Agr Univ, State Key Lab Agr Microbiol, Wuhan 430070, Peoples R China
7.Zhejiang Acad Agr Sci, Inst Agroprod Safety & Nutr, State Key Lab Managing Biot & Chem Threats Qual &, Hangzhou 310021, Peoples R China
8.Huazhong Agr Univ, Coll Plant Sci & Technol, Wuhan 430070, Peoples R China
关键词： 15-HETE; adaptive thermogenesis; adipose tissues; AMPK; chronic inflammation; microbes
期刊名称：ADVANCED SCIENCE （ 影响因子：14.1； 五年影响因子：15.6 ）
ISSN：
年卷期： 2024 年 11 卷 47 期
页码：
收录情况： SCI
摘要： Obesity represents a low-grade chronic inflammation status, which is associated with compromised adaptive thermogenesis. However, the mechanisms underlying the defective activation of thermogenesis in chronic inflammation remain unclear. Here, a chronic inflammatory model is first estabolished by injecting mice with low-dose lipopolysaccharide (LPS) before cold exposure, and then it is verified that LPS treatment can decrease the core body temperature of mice and alter the microbial distribution in epididymal white adipose tissue (eWAT). An adipose tissue-resident bacterium Sphingomonas paucimobilis is identified as a potential inhibitor on the activation of brown fat and browning of inguinal WAT, resulting in defective adaptive thermogenesis. Mechanically, LPS and S. paucimobilis inhibit the production and release of 15-HETE by suppressing its main metabolic enzyme 12 lipoxygenase (12-LOX) and 15- Hydroxyeicosatetraenoic acid (15-HETE) rescues the impaired thermogenesis. Interestingly, 15-HETE directly binds to AMP-activated protein kinase alpha (AMPK alpha) and elevates the phosphorylation of AMPK, leading to the activation of uncoupling protein 1 (UCP1) and mitochondrial oxidative phosphorylation (OXPHOS) complexes. Further analysis with human obesity subjects reveals that individuals with high body mass index displayed lower 15-HETE levels. Taken together, this work improves the understanding of how chronic inflammation impairs adaptive thermogenesis and provides novel targets for alleviating obesity.
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