Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk

Background and Aims: Metabolic syndrome (MS) is a progressive metabolic disease characterized by obesity and multiple metabolic disorders. Tryptophan (Trp) is an essential amino acid, and its metabolism is linked to numerous physiological functions and diseases. However, the mechanisms by which Trp...

Full description

Saved in:
Bibliographic Details
Main Authors: Jiayi Chen, Hao Yang, Yingjie Qin, Xinbo Zhou, Qingquan Ma
Format: Article
Language:English
Published: American Association for the Advancement of Science (AAAS) 2024-01-01
Series:Research
Online Access:https://spj.science.org/doi/10.34133/research.0515
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1846125958280511488
author Jiayi Chen
Hao Yang
Yingjie Qin
Xinbo Zhou
Qingquan Ma
author_facet Jiayi Chen
Hao Yang
Yingjie Qin
Xinbo Zhou
Qingquan Ma
author_sort Jiayi Chen
collection DOAJ
description Background and Aims: Metabolic syndrome (MS) is a progressive metabolic disease characterized by obesity and multiple metabolic disorders. Tryptophan (Trp) is an essential amino acid, and its metabolism is linked to numerous physiological functions and diseases. However, the mechanisms by which Trp affects MS are not fully understood. Methods and Results: In this study, experiments involving a high-fat diet (HFD) and fecal microbiota transplantation (FMT) were conducted to investigate the role of Trp in regulating metabolic disorders. In a mouse model, Trp supplementation inhibited intestinal farnesoid X receptor (FXR) signaling and promoted hepatic bile acid (BA) synthesis and excretion, accompanied by elevated levels of conjugated BAs and the ratio of non-12-OH to 12-OH BAs in hepatic and fecal BA profiles. As Trp alters the gut microbiota and the abundance of bile salt hydrolase (BSH)-enriched microbes, we collected fresh feces from Trp-supplemented mice and performed FMT and sterile fecal filtrate (SFF) inoculations in HFD-treated mice. FMT and SFF not only displayed lipid-lowering properties but also inhibited intestinal FXR signaling and increased hepatic BA synthesis. This suggests that the gut microbiota play a beneficial role in improving BA metabolism through Trp. Furthermore, fexaramine (a gut-specific FXR agonist) reversed the therapeutic effects of Trp, suggesting that Trp acts through the FXR signaling pathway. Finally, validation in a finishing pig model revealed that Trp improved lipid metabolism, enlarged the hepatic BA pool, and altered numerous glycerophospholipid molecules in the hepatic lipid profile. Conclusion: Our studies suggest that Trp inhibits intestinal FXR signaling mediated by the gut microbiota–BA crosstalk, which in turn promotes hepatic BA synthesis, thereby ameliorating MS.
format Article
id doaj-art-88f37947742d4e85826520f19debfd16
institution Kabale University
issn 2639-5274
language English
publishDate 2024-01-01
publisher American Association for the Advancement of Science (AAAS)
record_format Article
series Research
spelling doaj-art-88f37947742d4e85826520f19debfd162024-12-13T08:25:04ZengAmerican Association for the Advancement of Science (AAAS)Research2639-52742024-01-01710.34133/research.0515Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid CrosstalkJiayi Chen0Hao Yang1Yingjie Qin2Xinbo Zhou3Qingquan Ma4College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.Background and Aims: Metabolic syndrome (MS) is a progressive metabolic disease characterized by obesity and multiple metabolic disorders. Tryptophan (Trp) is an essential amino acid, and its metabolism is linked to numerous physiological functions and diseases. However, the mechanisms by which Trp affects MS are not fully understood. Methods and Results: In this study, experiments involving a high-fat diet (HFD) and fecal microbiota transplantation (FMT) were conducted to investigate the role of Trp in regulating metabolic disorders. In a mouse model, Trp supplementation inhibited intestinal farnesoid X receptor (FXR) signaling and promoted hepatic bile acid (BA) synthesis and excretion, accompanied by elevated levels of conjugated BAs and the ratio of non-12-OH to 12-OH BAs in hepatic and fecal BA profiles. As Trp alters the gut microbiota and the abundance of bile salt hydrolase (BSH)-enriched microbes, we collected fresh feces from Trp-supplemented mice and performed FMT and sterile fecal filtrate (SFF) inoculations in HFD-treated mice. FMT and SFF not only displayed lipid-lowering properties but also inhibited intestinal FXR signaling and increased hepatic BA synthesis. This suggests that the gut microbiota play a beneficial role in improving BA metabolism through Trp. Furthermore, fexaramine (a gut-specific FXR agonist) reversed the therapeutic effects of Trp, suggesting that Trp acts through the FXR signaling pathway. Finally, validation in a finishing pig model revealed that Trp improved lipid metabolism, enlarged the hepatic BA pool, and altered numerous glycerophospholipid molecules in the hepatic lipid profile. Conclusion: Our studies suggest that Trp inhibits intestinal FXR signaling mediated by the gut microbiota–BA crosstalk, which in turn promotes hepatic BA synthesis, thereby ameliorating MS.https://spj.science.org/doi/10.34133/research.0515
spellingShingle Jiayi Chen
Hao Yang
Yingjie Qin
Xinbo Zhou
Qingquan Ma
Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk
Research
title Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk
title_full Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk
title_fullStr Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk
title_full_unstemmed Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk
title_short Tryptophan Ameliorates Metabolic Syndrome by Inhibiting Intestinal Farnesoid X Receptor Signaling: The Role of Gut Microbiota–Bile Acid Crosstalk
title_sort tryptophan ameliorates metabolic syndrome by inhibiting intestinal farnesoid x receptor signaling the role of gut microbiota bile acid crosstalk
url https://spj.science.org/doi/10.34133/research.0515
work_keys_str_mv AT jiayichen tryptophanamelioratesmetabolicsyndromebyinhibitingintestinalfarnesoidxreceptorsignalingtheroleofgutmicrobiotabileacidcrosstalk
AT haoyang tryptophanamelioratesmetabolicsyndromebyinhibitingintestinalfarnesoidxreceptorsignalingtheroleofgutmicrobiotabileacidcrosstalk
AT yingjieqin tryptophanamelioratesmetabolicsyndromebyinhibitingintestinalfarnesoidxreceptorsignalingtheroleofgutmicrobiotabileacidcrosstalk
AT xinbozhou tryptophanamelioratesmetabolicsyndromebyinhibitingintestinalfarnesoidxreceptorsignalingtheroleofgutmicrobiotabileacidcrosstalk
AT qingquanma tryptophanamelioratesmetabolicsyndromebyinhibitingintestinalfarnesoidxreceptorsignalingtheroleofgutmicrobiotabileacidcrosstalk