Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue
Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue
复制标题
微生物群耗竭损害棕色脂肪组织的产热和白色脂肪组织的褐变
DOI：
10.1016/j.celrep.2019.02.015
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发表时间：
2019-03-05
期刊：
影响因子：
8.8
通讯作者：
Speakman, John R.
中科院分区：
文献类型：
--
作者：
Li, Baoguo;Li, Li;Speakman, John R.
肠道菌群和宿主之间的关系被认为有利于代谢稳态。棕色脂肪组织（BAT）和米色脂肪细胞促进产热，以维持宿主在寒冷暴露时的核心体温。然而，肠道菌群对产热过程的潜在影响尚不清楚。在这里，我们评估了BAT和白色脂肪组织（WAT）在缺乏肠道微生物群的小鼠中对温度挑战的反应。我们发现，通过使用不同的抗生素（ABX）鸡尾酒治疗或无菌（GF）小鼠的微生物群消耗，通过钝化解偶联蛋白1 （UCP1）的表达增加和减少WAT的褐变过程，损害了BAT的产热能力。灌胃细菌代谢物丁酸酯增加了abx处理小鼠的产热能力，逆转了这一缺陷。我们的研究结果表明，肠道微生物群有助于在寒冷环境中上调产热作用，这可能部分通过丁酸盐介导。
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 germfree (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.