腸內菌與代謝症候群

Gut Microbiota and Metabolic Syndrome

林家宏(Chia-Hung Lin) ； 林彥良(Yen-Liang Lin) ； 劉孟樽(Meng-Tsun Liu) ； 陳亭竹(Ting-Chu Chen) ； 湯舒宇(Shu-Yu Tang) ； 張恬君(Tien-Jyun Chang)

《臺大護理雜誌》 14卷2期 (2018/07) Pp. 5-11

https://doi.org/10.6740/NTUHJN.201807_14(2).0002

摘要

國內外代謝症候群盛行率不斷上升，隨之而來的心血管疾病以及死亡的風險亦上升，近年來腸內菌與代謝症候群的相關性被廣為研究，腸內菌本身會引響宿主的免疫外，其分泌的短鏈脂肪酸（shortchain fatty acids, SCFAs）與初級膽酸會刺激腸道內分泌細胞分泌出昇糖素類似胜肽（glucagon-like peptide 1, GLP-1）及胜肽YY（peptideYY, PYY），進一步調控血糖及脂肪代謝，及減少胃排空造成飽足感。腸內菌造成的全身發炎反應也可能導致第1型糖尿病的自體免疫反應，與第2型糖尿病的胰島素阻抗。此外，腸內菌分解形成及在肝臟代謝的氧化三甲胺（trimethylamine N-oxide, TMAO）也被發現與冠狀動脈心臟病有相關。目前糞便移植或益生菌對改善代謝症候群的證據仍有限，然而相關研究仍不斷進行，未來我們希望透過了解腸內菌的分布來給予個人化的診斷及治療，以達到精準醫療的目的。

並列摘要

The prevalence of metabolic syndrome has increased globally. The risk of cardiovascular disease and death has also increased. More evidence supports the relationship between microbiota and metabolic syndrome. The human immune system is influenced and modulated by bacteria, especially microbiota. The metabolites of microbiota include short-chain fatty acids (SCFAs) and primary bile acid. These molecules decrease blood sugar and slow gastric emptying time by stimulating the secretion of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). Furthermore, immune system defects and general inflammation lead to the pathogenesis of type 1 and type 2 diabetes mellitus. Recently, studies have shown that atherosclerosis was related to trimethylamine N-oxide (TMAO), which is generated by microbiota and metabolized in the liver. To date, the benefits of probiotic and stool transplantation have remained unknown. Thus, more research is needed. By increasing understanding of the map of microbiota, personalization and precision in medicine can be enabled in the field of microbiota and metabolic syndrome.