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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.
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•Mice lacking gut microbiota have impaired UCP1-dependent thermogenesis in cold•These effects are replicated in germ-free mice treated with CL-316243•IL-4 has no differential effect on energy metabolism in either control or ABX mice•Gavage of ABX mice with butyrate partially rescues the effects on BAT recruitment
Li et al. use different antibiotic recipes and germ-free mice to demonstrate the dependence of UCP1-dependent thermogenesis in the cold on the presence of a healthy gut microbiome. Gavage with butyrate partly rescues the effect, indicating a role for this molecule in normal thermogenic responses to low temperature.