Cold Stress Activates the UCP3 Pathway via Gut Microbiota in Piglet

BackgroundThe gut microbiota plays a key role in the host metabolic thermogenesis by activating uncoupling protein 1 (UCP1) and increasing the browning process of white adipose tissue, especially in a cold environment. However, the crosstalk between gut microbiota and pigs, which lack functional UCP1 making them susceptible to cold, has rarely been illustrated. We used male piglets as a model to evaluate the host response to cold stress via the gut microbiota. ResultsWe found that host thermogenesis and insulin resistance with increased serum metabolites, such as glycocholic acid (GCA), glycochenodeoxycholate (GCDCA), and chenodeoxycholate (CDCA), and altered cecal microbiota compositions and functions under cold stress. Using transcriptomics technology, we found that cytochrome P450, family 8, subfamily b, polypeptide 1 (CYP8B1), FXR, FFAR2, and FFAR3, which are related to bile acid and short-chain fatty acid metabolism, increased in the liver under cold stress. In addition, the fat lipolysis genes CLPS, PNLIPRP1, carnitine palmitoyltransferase 1B (CPT1B), and uncoupling protein 3 (UCP3) were significantly increased in the fat of piglets under cold stress. However, microbiota depletion via treatment with mixed antibiotics weakened the effect on the genes CYP8B1, FFAR2, FFAR3, and CPT1B genes, indicating that the gut microbiota plays important roles in the host thermogenesis. ConclusionsOur results demonstrate that the gut microbiota-blood-liver and fat axis may regulate thermogenesis during cold acclimation in piglets.