Instead of stamping your feet and rubbing your hands together when it’s cold, it might be better to “fire-up” the gut microbiota to increase your core temperature. While the influx of research over the past several years has pointed to the overwhelming importance of the microbiome in maintaining health and preventing disease onset, few studies have addressed the role the body’s microbial environment plays in thermoregulation—the way many animals regulate their core body temperature. Now, a team of investigators from the Institute of Genetics and Developmental Biology at the Chinese Academy of Sciences has new evidence that reveals the important role for the gut microbiota in thermoregulation.

Findings from the new study were published recently in Cell Reports through an article titled “Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue.”

During cold exposure, it is well established that animals sustain their body temperature by activating heat production from a specialized tissue known as Brown Adipose Tissue (BAT) and promoting “browning” of white adipose tissue.

To evaluate the function of gut microbiota in the activation of BAT, the research team used different antibiotic concoctions to eradicate gut microbiota. They subsequently found that animals lacking gut microbiota had impaired thermoregulation. Moreover, the results were also confirmed in germ-free mice.

Li et al., used 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. [Li et al., 2019, Cell Reports 26, 2720–2737]
“We evaluated how BAT and white adipose tissue (WAT) responded to temperature challenges in mice lacking gut microbiota,” the authors wrote. “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.”

The researchers surmised that this effect could be because, in the absence of an intact microbiome, the animal is unable to digest sufficient quantities of food to meet elevated energy demands in the cold, and the impact on BAT is a secondary effect. Moreover, since the team also showed that they could reverse the thermogenic deficit in the ABX-treated mice, they suggest that this evidence support their hypothesis that the microbiota plays an important signaling role in the process that stimulates cold-induced thermogenesis.

“Our results indicate that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated via butyrate,” the authors concluded.

Importantly, this research adds to the expanding areas of physiology and health that are impacted by the gut microbiome. Although the work was conducted in mice, and extensions to humans must be made cautiously, it may have several health implications. In particular, elderly people have many problems raising an adequate thermoregulation response to the cold, which makes them susceptible to hypothermia. It will be interesting to discover if known changes in the human microbiome with age contribute to this effect, and if modulating the age-related changes in the microbiome will afford elderly people more protection.

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