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Prevention of Vascular Inflammation by Pterostilbene via Trimethylamine‐ N ‐Oxide Reduction and Mechanism of Microbiota Regulation
Author(s) -
Koh YenChun,
Li Shiming,
Chen PeiYu,
Wu JiaChing,
Kalyanam Nagabhushanam,
Ho ChiTang,
Pan MinHsiung
Publication year - 2019
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201900514
Subject(s) - pterostilbene , trimethylamine n oxide , inflammation , gut flora , carnitine , metabolite , tumor necrosis factor alpha , biology , microbiology and biotechnology , chemistry , biochemistry , immunology , trimethylamine , resveratrol
Scope A gut‐microbiota‐dependent metabolite of L‐carnitine, trimethylamine‐ N ‐oxide (TMAO), has been recently discovered as an independent and dose‐dependent risk factor for cardiovascular disease (CVD). This study aims to investigate the effects of pterostilbene on reducing TMAO formation and on decreasing vascular inflammation in carnitine‐feeding mice. Methods and results C57BL/6 mice are treated with 1.3% carnitine in drinking water with or without pterostilbene supplementation. Using LC‐MS/MS, the result shows that mice treated with 1.3% carnitine only significantly increased the plasma TMAO and pterostilbene supplementation group can reverse it. Additionally, pterostilbene decreases hepatic flavin monooxygenase 3 (FMO3) mRNA levels compared to carnitine only group. It appears that pterostilbene can alter host physiology and create an intestinal microenvironment favorable for certain gut microbiota. Gut microbiota analysis reveals that pterostilbene increases the abundance of Bacteroides . Further, pterostilbene decreases mRNA levels of vascular inflammatory markers tumor necrosis factor‐α (TNF‐α), vascular cell adhesion molecule 1 (VCAM‐1), and E‐selectin). Conclusion These data suggest that amelioration of carnitine‐induced vascular inflammation after consumption of pterostilbene is partially mediated via modulation of gut microbiota composition and hepatic enzyme FMO3 gene expression.