犬尿氨酸
失调
犬尿氨酸途径
分解代谢
嗜铬细胞
免疫系统
喹啉酸
免疫学
血清素
焦虑
生物
色氨酸
医学
肠道菌群
炎症
吲哚胺2,3-双加氧酶
内科学
生物化学
酶
精神科
氨基酸
受体
作者
Alper Evrensel,Barış Önen Ünsalver,Mehmet Emin Ceylan
标识
DOI:10.1007/978-981-32-9705-0_10
摘要
Anxiety disorders are a complex set of illnesses in which genetic factors, particularly stress, play a role in the etiopathogenesis. In recent years, inflammation and intestinal microbiota have also been included in this complex network of relationships. The functions associated with tryptophan catabolism and serotonin biosynthesis have long been associated with anxiety disorders. Tryptophan catabolism progresses toward the path of the kynurenine in the presence of stress and inflammation. The catabolism of kynurenine is a pathway in which many enzymes play a role and a large number of catabolites with neuroactive properties occur. The body's serotonin biosynthesis is primarily performed by enterochromaffin cells located in the intestines. A change in the intestinal microbiota composition (dysbiosis) directly affects the serotonin biosynthesis. Stress, unhealthy nutrition, and the use of antibiotics cause dysbiosis. In the light of this new perspective, the role of dysbiosis-induced inflammation and kynurenine pathway catabolites activated sequentially come into prominence in the etiopathogenesis of anxiety disorders.
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