State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing, 100049, China.
Microb Biotechnol. 2022 Mar;15(3):817-831. doi: 10.1111/1751-7915.13793. Epub 2021 Mar 17.
Endothermic mammals have a high energy cost to maintain a stable and high body temperature (T , around 37°C). Thyroid hormones are a major regulator for energy metabolism and T . The gut microbiota is involved in modulating host energy metabolism. However, whether the interaction between the gut microbiota and thyroid hormones is involved in metabolic and thermal regulations is unclear. We hypothesized that thyroid hormones via an interaction with gut microbiota orchestrate host thermogenesis and T . l-thyroxine-induced hyperthyroid Mongolian gerbils (Meriones unguiculatus) increased resting metabolic rate (RMR) and T , whereas Methimazole-induced hypothyroid animals decreased RMR. Both hypothyroid and hyperthyroid animals differed significantly in faecal bacterial community. Hyperthyroidism increased the relative abundance of pathogenic bacteria, such as Helicobacter and Rikenella, and decreased abundance of beneficial bacteria Butyricimonas and Parabacteroides, accompanied by reduced total bile acids and short-chain fatty acids. Furthermore, the hyperthyroid gerbils transplanted with the microbiota from control donors increased type 2 deiodinase (DIO2) expression in the liver and showed a greater rate of decline of both serum T3 and T4 levels and, consequently, a more rapid recovery of normal RMR and T . These findings indicate that thyroid hormones regulate thermogenesis depending on gut microbiota and colonization with normal microbiota by caecal microbial transplantation attenuates hyperthyroid-induced thermogenesis. This work reveals the functional consequences of the gut microbiota-thyroid axis in controlling host metabolic physiology and T in endotherms.
温血哺乳动物维持稳定和高体温（T，约 37°C）的能量成本很高。甲状腺激素是能量代谢和 T 的主要调节剂。肠道微生物群参与调节宿主的能量代谢。然而，肠道微生物群和甲状腺激素之间的相互作用是否参与代谢和热调节尚不清楚。我们假设，甲状腺激素通过与肠道微生物群的相互作用来协调宿主的产热和 T。l-甲状腺素诱导的甲状腺功能亢进蒙古沙鼠（Meriones unguiculatus）增加静息代谢率（RMR）和 T，而甲巯咪唑诱导的甲状腺功能减退动物则降低 RMR。甲状腺功能减退和甲状腺功能亢进的动物粪便细菌群落有显著差异。甲状腺功能亢进症增加了致病性细菌的相对丰度，如 Helicobacter 和 Rikenella，而有益细菌 Butyricimonas 和 Parabacteroides 的丰度降低，同时总胆汁酸和短链脂肪酸减少。此外，接受来自对照供体的微生物群移植的甲状腺功能亢进沙鼠增加了肝脏中的 2 型脱碘酶（DIO2）表达，并表现出血清 T3 和 T4 水平下降更快，因此恢复正常 RMR 和 T 的速度更快。这些发现表明，甲状腺激素根据肠道微生物群调节产热，而通过盲肠微生物群移植定植正常微生物群可减轻甲状腺功能亢进引起的产热。这项工作揭示了肠道微生物群-甲状腺轴在控制内温动物宿主代谢生理学和 T 中的功能后果。
