Cecal microbial transplantation attenuates hyperthyroid-induced thermogenesis in Mongolian gerbils.
Cecal microbial transplantation attenuates hyperthyroid-induced thermogenesis in Mongolian gerbils.
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盲肠微生物移植减弱蒙古沙鼠甲状腺功能亢进诱导的生热作用
DOI：
10.1111/1751-7915.13793
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发表时间：
2022-03
影响因子：
5.7
通讯作者：
Wang DH
中科院分区：
文献类型：
--
作者：
Khakisahneh S;Zhang XY;Nouri Z;Wang DH
吸热型哺乳动物有很高的能量消耗来维持稳定和高的体温（Tb，约37°C）。甲状腺激素是能量代谢和结核病的主要调节剂。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涉及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协调宿主产热和Tb。l-甲状腺素诱导的甲状腺功能亢进蒙古沙鼠（长爪沙鼠）增加静息代谢率（RMR）和Tb，而甲巯咪唑诱导的甲状腺功能减退动物降低RMR。甲状腺功能减退和甲状腺功能亢进动物粪便细菌群落差异显着。甲状腺功能亢进症增加了致病菌的相对丰度，如螺杆菌和Rikenella，并减少了有益细菌Butyricimonas和Parabacteroides的丰度，伴随着总胆汁酸和短链脂肪酸的减少。此外，移植有来自对照供体的微生物群的甲状腺机能亢进沙鼠增加了肝脏中的2型脱碘酶（DIO 2）表达，并显示出血清T3和T4水平的更大下降速率，因此，正常RMR和Tb的恢复更快。这些发现表明，甲状腺激素依赖于肠道微生物群调节产热，并且通过盲肠微生物移植与正常微生物群的定殖减弱了甲状腺功能亢进诱导的产热。这项工作揭示了肠道微生物群-甲状腺轴在控制宿主代谢生理学和吸热动物中Tb的功能后果。在本文中，我们表明，甲状腺功能亢进症表现出静息代谢率（RMR）和体温（T B）的增加，并与肠道微生物群落紊乱，增加相对丰度的致病菌，如螺杆菌和Rikenella，和减少丰度的有益细菌丁酸单胞菌和副杆菌。盲肠微生物移植正常微生物群定植通过调节2型脱碘酶（DIO 2）表达减弱甲状腺功能亢进诱导的产热作用。这些发现强调了肠道微生物群-甲状腺轴在控制宿主代谢生理学和T B方面的功能后果。
Endothermic mammals have a high energy cost to maintain a stable and high body temperature (Tb , around 37°C). Thyroid hormones are a major regulator for energy metabolism and Tb . 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 Tb . l‐thyroxine‐induced hyperthyroid Mongolian gerbils (Meriones unguiculatus) increased resting metabolic rate (RMR) and Tb , 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 Tb . 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 Tb in endotherms. In this paper, we demonstrate that hyperthyroidism showed increases in resting metabolic rate (RMR) and body temperature (T b ), and were associated with a disturbed gut microbial community, with increased relative abundances of pathogenic bacteria, such as Helicobacter and Rikenella, and decreased abundances of beneficial bacteria Butyricimonas and Parabacteroides. Colonization with normal microbiota by caecal microbial transplantation attenuated hyperthyroid‐induced thermogenesis through regulation of type 2 deiodinase (DIO2) expression. These findings emphasize the functional consequences of the gut microbiota‐thyroid axis in controlling host metabolic physiology and T b .
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