State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, PRC; University of Chinese Academy of Sciences, Beijing 100049, PRC.
State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, PRC; University of Chinese Academy of Sciences, Beijing 100049, PRC; Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen AB24 2TZ, UK.
Cell Rep. 2019 Mar 5;26(10):2720-2737.e5. doi: 10.1016/j.celrep.2019.02.015.
The relation between gut microbiota and the host has been suggested to benefit metabolic homeostasis. Brown adipose tissue (BAT) and beige adipocytes facilitate thermogenesis to maintain host core body temperature during cold exposure. However, the potential impact of gut microbiota on the thermogenic process is confused. Here, we evaluated how BAT and white adipose tissue (WAT) responded to temperature challenges in mice lacking gut microbiota. We found that microbiota depletion via treatment with different cocktails of antibiotics (ABX) or in germ-free (GF) mice impaired the thermogenic capacity of BAT by blunting the increase in the expression of uncoupling protein 1 (UCP1) and reducing the browning process of WAT. Gavage of the bacterial metabolite butyrate increased the thermogenic capacity of ABX-treated mice, reversing the deficit. Our results indicate that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated via butyrate.
肠道微生物群与宿主之间的关系被认为有助于代谢稳态。棕色脂肪组织(BAT)和米色脂肪细胞促进产热,以在寒冷暴露期间维持宿主核心体温。然而,肠道微生物群对产热过程的潜在影响尚不清楚。在这里,我们评估了在缺乏肠道微生物群的小鼠中,BAT 和白色脂肪组织(WAT)如何对温度挑战做出反应。我们发现,通过使用不同的抗生素鸡尾酒(ABX)或在无菌(GF)小鼠中处理来耗尽微生物群,通过抑制解偶联蛋白 1(UCP1)表达的增加和减少 WAT 的褐变过程来削弱 BAT 的产热能力。灌胃细菌代谢物丁酸盐增加了 ABX 处理小鼠的产热能力,从而逆转了这种缺陷。我们的结果表明,肠道微生物群有助于在寒冷环境中上调产热,而这可能部分是通过丁酸盐介导的。