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Hyperuricemia is associated with impaired intestinal permeability in mice

Authors :
Peng Zhao
Pengjun Wang
Xuena Cui
Xiu Liu
Guangtao Wang
Wan Yang
Daxing Xu
Guanpin Yang
Zenglan Wang
Shichao Xing
Xiaofeng Wang
Xiaomin Yang
Qiulan Lv
Zhiyuan Li
Source :
American journal of physiology. Gastrointestinal and liver physiology. 317(4)
Publication Year :
2019

Abstract

Hyperuricemia is associated with many metabolic diseases. However, the underlying mechanism remains unknown. The gut microbiota has been demonstrated to play significant roles in the immunity and metabolism of the host. In the present study, we constructed a hyperuricemic mouse model to investigate whether the metabolic disorder caused by hyperuricemia is related to intestinal dysbiosis. A significantly increased intestinal permeability was detected in hyperuricemic mice. The difference in microflora between wild-type and hyperuricemic mice accompanies the translocation of gut microbiota to the extraintestinal tissues. Such a process is followed by an increase in innate immune system activation. We observed increased LPS and TNF-α levels in the hyperuricemic mice, indicating that hyperuricemic mice were in a state of low-grade systemic inflammation. In addition, hyperuricemic mice presented early injury of parenteral tissue and disordered lipid metabolism. These findings suggest that intestinal dysbiosis due to an impaired intestinal barrier may be the key cause of metabolic disorders in hyperuricemic mice. Our findings should aid in paving a new way of preventing and treating hyperuricemia and its complications. NEW & NOTEWORTHY Hyperuricemia is associated with many metabolic diseases. However, the underlying mechanism remains unknown. We constructed a hyperuricemic mouse model to explore the relationship between intestinal dysbiosis and metabolic disorder caused by hyperuricemia.

Details

ISSN :
15221547
Volume :
317
Issue :
4
Database :
OpenAIRE
Journal :
American journal of physiology. Gastrointestinal and liver physiology
Accession number :
edsair.doi.dedup.....3c38e46c21ce97b2f2f830439937b7b2