Regulation of bile acid metabolism-related signaling pathways by gut microbiota in diseases

Over the past decade, there has been increasing attention on the interaction between microbiota and bile acid metabolism. Bile acids are not only involved in the metabolism of nutrients, but are also important in signal transduction for the regulation of host physiological activities. Microbial-regu...

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Bibliographic Details
Published in:Journal of Zhejiang University. B. Science 2019-10, Vol.20 (10), p.781-792
Main Authors: Jia, Er-teng, Liu, Zhi-yu, Pan, Min, Lu, Jia-feng, Ge, Qin-yu
Format: Article
Language:English
Subjects:
Acids
Bile
Bile acids
Bile Acids and Salts - metabolism
Biomedical and Life Sciences
Biomedicine
Diseases
Gastrointestinal Microbiome
Humans
Inflammation - metabolism
Intestinal microflora
Metabolic Syndrome - metabolism
Metabolism
Microbiota
Microorganisms
Nutrients
Pathogenesis
Receptors, Calcitriol - physiology
Receptors, Cytoplasmic and Nuclear - physiology
Receptors, G-Protein-Coupled - physiology
Review
Signal transduction
Signal Transduction - physiology
Signaling
Vitamin D
Vitamin D receptors
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Summary:Over the past decade, there has been increasing attention on the interaction between microbiota and bile acid metabolism. Bile acids are not only involved in the metabolism of nutrients, but are also important in signal transduction for the regulation of host physiological activities. Microbial-regulated bile acid metabolism has been proven to affect many diseases, but there have not been many studies of disease regulation by microbial receptor signaling pathways. This review considers findings of recent research on the core roles of farnesoid X receptor (FXR), G protein-coupled bile acid receptor (TGR5), and vitamin D receptor (VDR) signaling pathways in microbial–host interactions in health and disease. Studying the relationship between these pathways can help us understand the pathogenesis of human diseases, and lead to new solutions for their treatments.
ISSN:1673-1581
1862-1783
DOI:10.1631/jzus.B1900073