Academic Journal

Adipose Tissue‐Resident Sphingomonas Paucimobilis Suppresses Adaptive Thermogenesis by Reducing 15‐HETE Production and Inhibiting AMPK Pathway.

التفاصيل البيبلوغرافية
العنوان: Adipose Tissue‐Resident Sphingomonas Paucimobilis Suppresses Adaptive Thermogenesis by Reducing 15‐HETE Production and Inhibiting AMPK Pathway.
المؤلفون: Zhu, Yucheng1 (AUTHOR), Yang, Ruiqi1 (AUTHOR), Deng, Zhangchao1 (AUTHOR), Deng, Bohua1 (AUTHOR), Zhao, Kun2 (AUTHOR), Dai, Chen3 (AUTHOR), Wei, Gang4 (AUTHOR), Wang, YanJiang5 (AUTHOR), Zheng, Jinshui6 (AUTHOR), Ren, Zhuqing1 (AUTHOR), Lv, Wentao7 (AUTHOR), Xiao, Yingping7 (AUTHOR) xiaoyp@zaas.ac.an, Mei, Zhinan8 (AUTHOR) meizhinan@mail.hzau.edu.cn, Song, Tongxing1 (AUTHOR) songtongxing@mail.hzau.edu.cn
المصدر: Advanced Science. 12/18/2024, Vol. 11 Issue 47, p1-17. 17p.
مصطلحات موضوعية: *WHITE adipose tissue, *BROWN adipose tissue, *BODY mass index, *AMP-activated protein kinases, *ADIPOSE tissues
مستخلص: 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 α (AMPKα) 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. [ABSTRACT FROM AUTHOR]
قاعدة البيانات: Academic Search Index
الوصف
تدمد:21983844
DOI:10.1002/advs.202310236