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饮食、肠道微生物群与非酒精性脂肪性肝病:同一轴心的三个部分。

Diet, Gut Microbiota and Non-Alcoholic Fatty Liver Disease: Three Parts of the Same Axis.

机构信息

Unitat de Nutrició i Salut, Centre Tecnològic de Catalunya, Eurecat, 43204 Reus, Spain.

Department of Biochemistry and Biotechnology, Universitat Rovira i Virgili, Nutrigenomics Research Group, 43007 Tarragona, Spain.

出版信息

Cells. 2020 Jan 10;9(1):176. doi: 10.3390/cells9010176.

Abstract

Non-Alcoholic Fatty Liver Disease (NAFLD) is the most common liver disease in the world. NAFLD is principally characterized by an excessive fat accumulation in the hepatocytes. Diet is considered as one of the main drivers to modulate the composition of gut microbiota, which participate in different processes, affecting human metabolism. A disruption in the homeostasis of gut microbiota may lead to dysbiosis, which is commonly reflected by a reduction of the beneficial species and an increment in pathogenic microbiota. Gut and liver are in close relation due to the anatomical and functional interactions led by the portal vein, thus altered intestinal microbiota might affect liver functions, promoting inflammation, insulin resistance and steatosis, which is translated into NAFLD. This review will highlight the association between diet, gut microbiota and liver, and how this axis may promote the development of NAFLD progression, discussing potential mechanisms and alterations due to the dysbiosis of gut microbiota. Finally, it will revise the variations in gut microbiota composition in NAFLD, and it will focus in specific species, which directly affect NAFLD progression.

摘要

非酒精性脂肪性肝病 (NAFLD) 是世界上最常见的肝脏疾病。NAFLD 的主要特征是肝细胞内脂肪过度堆积。饮食被认为是调节肠道微生物群落组成的主要驱动因素之一,肠道微生物群落参与了不同的过程,影响着人类的新陈代谢。肠道微生物群落的平衡失调可能导致微生态失调,通常表现为有益物种的减少和病原微生物的增加。由于门静脉的解剖和功能相互作用,肠道和肝脏密切相关,因此改变的肠道微生物群落可能会影响肝脏功能,促进炎症、胰岛素抵抗和脂肪变性,从而导致 NAFLD。本综述将重点介绍饮食、肠道微生物群和肝脏之间的关系,以及该轴如何促进 NAFLD 进展,讨论由于肠道微生物群落失调而导致的潜在机制和改变。最后,它将回顾 NAFLD 中肠道微生物群落组成的变化,并重点关注直接影响 NAFLD 进展的特定物种。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/327d/7016763/3bba1df0c385/cells-09-00176-g001.jpg

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