Abstract
Cholesterol is an essential lipid in vertebrates, but excess blood cholesterol promotes atherosclerosis. In the liver, cholesterol is metabolized to bile acids by cytochrome P450, family 7, subfamily a, polypeptide 1 (CYP7A1), the transcription of which is negatively regulated by the ERK pathway. Fibroblast growth factor 21 (FGF21), a hepatokine, induces ERK phosphorylation and suppresses Cyp7a1 transcription. Taurine, a sulfur-containing amino acid, reportedly promotes cholesterol metabolism and lowers blood and hepatic cholesterol levels. However, the influence of long-term feeding of taurine on cholesterol levels and metabolism remains unclear. Here, to evaluate the more chronic effects of taurine on cholesterol levels, we analyzed mice fed a taurine-rich diet for 14–16 weeks. Long-term feeding of taurine lowered plasma cholesterol and bile acids without significantly changing other metabolic parameters, but hardly affected these levels in the liver. Moreover, taurine upregulated Cyp7a1 levels, while downregulated phosphorylated ERK and Fgf21 levels in the liver. Likewise, taurine-treated Hepa1-6 cells, a mouse hepatocyte line, exhibited downregulated Fgf21 levels and upregulated promoter activity of Cyp7a1. These results indicate that taurine promotes cholesterol metabolism by suppressing the FGF21/ERK pathway followed by upregulating Cyp7a1 expression. Collectively, this study shows that long-term feeding of taurine lowers both plasma cholesterol and bile acids, reinforcing that taurine effectively prevents hypercholesterolemia.
Highlights
These results indicate that taurine exerted little influence on whole-body metabolism in this model
These findings suggest that taurine strongly induced the catabolism of cholesterol and bile acid transported into the liver, resulting in their lowered plasma levels
We demonstrated that long-term feeding of taurine lowered plasma cholesterol and suppressed the Fibroblast growth factor 21 (FGF21)/extracellular signalregulated kinase (ERK) pathway in mice
Summary
Cholesterol is an essential lipid for lipid bilayers and biosynthesis of steroid hormones. Obese patients often show a high blood cholesterol level, which promotes atherosclerosis [1,2]. The blood levels of cholesterol are strictly regulated mainly by the liver, which releases cholesterol in the form of very low-density lipoprotein (VLDL) and takes in cholesterol through the low-density-lipoprotein (LDL) receptor [3]. Cholesterol is converted to bile acids, including cholic acids and deoxycholic acids, in the liver; steroid hormones, including sex hormones, in the testes or ovaries; and glucocorticoid, in the adrenal cortex
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