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作 者:郁霞青 吕中伟[1] 李丹[1] Yu Xiaqing;Lyu Zhongwei;Li Dan(Department of Nuclear Medicine,Tenth People′s Hospital Affiliated to Tongji University,Shanghai 200072,China)
机构地区:[1]同济大学附属第十人民医院核医学科,上海200072
出 处:《中华核医学与分子影像杂志》2022年第3期181-185,共5页Chinese Journal of Nuclear Medicine and Molecular Imaging
摘 要:碘是人体必需的微量元素,胃肠道摄入是人体获取碘的主要途径。肠道包含的万亿数量级的微生物对于人体物质能量代谢及基因信息调控有着十分重要的影响。肠道微生物或其代谢产物可通过循环系统作用于甲状腺(即"肠-甲状腺轴"),对甲状腺的碘代谢进行潜在调控。该文综述了肠道微生物对肠内碘摄取的影响及其对甲状腺细胞表面钠/碘同向转运体(NIS)表达及活性的调控,探讨了肠道微生物参与甲状腺碘代谢的潜在调控机制。肠道微生物影响甲状腺碘代谢的直接因素包括脂多糖、短链脂肪酸、微生物肽段或蛋白质等,通过影响核因子kappa B通路、参与组蛋白乙酰化修饰或抗原抗体反应等方式影响甲状腺NIS的表达或活性;间接因素包括肠道微生物改变细胞内环境,从而通过调控甲状腺特异转录因子的水平及调节促甲状腺激素及其受体介导的信号通路等方式影响甲状腺细胞内外碘离子的转运。Iodine is an essential trace element in the human body,and the gastrointestinal tract is the main way for the body to intake iodine.The intestinal tract contains trillions of microorganisms that have important impacts on the substance-energy metabolism and the genetic information processing in the human body.Gut microbiota or their metabolites can act on the thyroid through the circulatory system(namely the"gut-thyroid axis"),thus potentially regulating iodine metabolism in thyroid.This article reviews the effects of gut microbiota on intestinal iodine uptake,as well as the effects of gut microbiota and their metabolites on the expression and activity of sodium iodide symporter(NIS)in thyroid cells,thus exploring the potential regulatory mechanisms of gut microbiota that involved in thyroid iodine metabolism.Potential factors affecting thyroid iodine metabolism by gut microbiota include the direct and the indirect factors.The direct factors include lipopolysaccharides,short-chain fatty acids,microbial peptides,and microbial proteins,which may affect the expression or activity of NIS in thyroid by regulating the nuclear factor kappa-B pathway,histone acetylation modifications,or antigen-antibody reactions.The indirect factors include the altered cellular environment that effected by gut microbiota which can further affect the transport of iodine ions in thyroid cells by manners like regulating the levels of thyroid-specific transcription factors and regulating the signal pathways mediated by thyroid-stimulating hormone and its receptor.
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