High-fat diet-induced obesity is characterized by low-grade inflammation, which has been linked to gut microbiota dysbiosis. We hypothesized that quercetin supplementation would alter gut microbiota and reduce inflammation in obese mice. Male C57BL/6J mice, 4 weeks of age, were divided into 3 groups, including a low-fat diet group, a high-fat diet (HFD) group, and a high-fat diet plus quercetin (HFD+Q) group.The mice in HFD+Q group were given 50 mg per kg BW quercetin by gavage for 20 weeks. The body weight, fat accumulation, gut barrier function, glucose tolerance,
Background
Indole-3-propionic acid (IPA), a microbiota-produced tryptophan metabolite, has been shown to exhibit cardioprotective effects in animal models. However, the relation of IPA with cardiovascular risk in humans is currently unknown.
Objectives
This prospective study aimed to investigate whether plasma tryptophan and IPA levels are associated with decreased risks of mortality.
Methods
Ultrahigh-performance liquid chromatography–tandem mass spectrometry was used to measure plasma tryptophan and IPA levels in 1,829 coronary artery disease (CAD) patients. Cox proportional hazards regression models were used to estimate the associations between tryptophan and IPA levels and the risk of cardiovascular and all-cause mortality.
Results
During the median 9.2-year follow-up, 424 all-cause deaths occurred, of which 272 were cardiovascular deaths. Plasma tryptophan and IPA levels were significantly associated with a reduced risk of cardiovascular and all-cause mortality. CAD patients with the highest quartile of tryptophan and IPA levels had multivariable-adjusted hazard ratios of 0.62 (95% confidence interval [CI], 0.43, 0.89) and 0.71 (95% CI 0.50, 0.99), respectively, for cardiovascular mortality and 0.67 (95% CI, 0.50, 0.90) and 0.75 (95%CI 0.57, 0.99), respectively, for all-cause mortality compared with that in CAD patients in the lowest quartile. After multivariable adjustments, one standard deviation increase in the continuous plasma tryptophan and IPA levels were respectively associated with 16% and 14% decreases in the risk of cardiovascular mortality and with 13% and 14% decreases in the risk of all-cause mortality. Restricted cubic splines displayed linear associations between plasma tryptophan and IPA levels and cardiovascular and all-cause mortality among CAD patients.
Conclusions
Our findings suggest that plasma tryptophan and IPA levels are significantly associated with decreased risk of cardiovascular and all-cause mortality in CAD patients. Further studies are needed to determine the clinical diagnostic and therapeutic values of tryptophan and IPA levels on the risk of mortality among CAD patients.
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