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益生菌乳杆菌通过减少宿主肠道脂肪酸吸收来预防肝脂肪变性的保护机制。

A protective mechanism of probiotic Lactobacillus against hepatic steatosis via reducing host intestinal fatty acid absorption.

机构信息

Laboratory of Mitochondrial and Metabolic Diseases, Department of Health Sciences and Technology, GAIHST, Gachon University, Incheon, Korea.

Department of Medicine, Gachon University School of Medicine, Incheon, Korea.

出版信息

Exp Mol Med. 2019 Aug 13;51(8):1-14. doi: 10.1038/s12276-019-0293-4.

Abstract

The gut microbiome has been known to contribute up to ~30% of the energy absorption of the host. Although various beneficial mechanisms of probiotics have been suggested for non-alcoholic fatty liver disease (NAFLD), whether and which probiotics impact the host's intestinal energy absorption have not yet been quantitatively studied. Here, we suggest a novel mechanism of probiotics against NAFLD, in which Lactobacillus rhamnosus GG, the most common probiotic, shares intestinal fatty acids and prevents the development of diet-induced hepatic steatosis. By using quantitative methods (radioactive tracers and LC-MS) under both in vitro and in vivo conditions, we found that bacteria and hosts competed for fatty acid absorption in the intestine, resulting in decreased weight gain, body fat mass, and hepatic lipid accumulation without differences in calorie intake and excretion in mice fed the probiotic bacteria.

摘要

肠道微生物组被认为可以贡献宿主能量吸收的高达 30%。尽管已经提出了各种益生菌对非酒精性脂肪性肝病(NAFLD)的有益机制,但益生菌是否以及哪些益生菌会影响宿主的肠道能量吸收尚未进行定量研究。在这里,我们提出了益生菌对抗非酒精性脂肪性肝病的一种新机制,其中最常见的益生菌鼠李糖乳杆菌 GG 共享肠道脂肪酸并防止饮食诱导的肝脂肪变性的发展。通过在体外和体内条件下使用定量方法(放射性示踪剂和 LC-MS),我们发现细菌和宿主在肠道中争夺脂肪酸吸收,导致体重增加、体脂肪质量和肝脂质积累减少,而喂食益生菌的小鼠的卡路里摄入量和排泄没有差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b659/6802638/9f7895a0fea8/12276_2019_293_Fig1_HTML.jpg

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