Cell Reports
Abstract
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.
论文编号: | DOI:10.1016/j.celrep.2019.02.015 |
论文题目: | Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue |
英文论文题目: | Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue |
第一作者: | Baoguo Li, Li Li, Min Li, Sin Man Lam, Guanlin Wang, Yingga Wu, Hanlin Zhang, Chaoqun Niu, Xueying Zhang, Xue Liu, Catherine Hambly, Wanzhu Jin, Guanghou Shui, John R. Speakman |
英文第一作者: | Baoguo Li, Li Li, Min Li, Sin Man Lam, Guanlin Wang, Yingga Wu, Hanlin Zhang, Chaoqun Niu, Xueying Zhang, Xue Liu, Catherine Hambly, Wanzhu Jin, Guanghou Shui, John R. Speakman |
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发表年度: | 2019-03-06 |
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摘要: | 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. |
英文摘要: | 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. |
刊物名称: | Cell Reports |
英文刊物名称: | Cell Reports |
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其它备注: | Baoguo Li, Li Li, Min Li, Sin Man Lam, Guanlin Wang, Yingga Wu, Hanlin Zhang, Chaoqun Niu, Xueying Zhang, Xue Liu, Catherine Hambly, Wanzhu Jin, Guanghou Shui, John R. Speakman. Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue. Cell Reports DOI:10.1016/j.celrep.2019.02.015 |
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