Researchers from the Peking University School of Medicine and the University of Houston have confirmed in new research that gene defects in the Farnesoid X receptor (FXR) can impair urine concentration. The research results were published in the Proceedings of the American Academy of Sciences (PNAS).
Professor Youfei Guan of the Peking University School of Medicine and Professor Jan-ke Gustafsson of the University of Houston are co-corresponding authors of this paper. Professor Guan's main research direction uses transgenes, gene targeting and disease animal models to study the prostaglandin and its receptors and metabolic nuclear receptors in the pathogenesis and treatment of diabetes, hypertension, lipid metabolism disorders, obesity and related renal complications effect.
FXR is a ligand-activated transcription factor that belongs to the nuclear receptor superfamily. FXR is mainly expressed in the liver and small intestine. It plays an important role in the regulation of the expression of a series of genes in bile acid metabolism, lipid metabolism, sugar metabolism, liver protection, intestinal bacterial growth and atherosclerosis. . Therefore, FXR is expected to become a drug target for the treatment of a series of metabolic diseases such as cholestasis, hypertriglyceridemia, and diabetes. In addition, the study found that FXR is also expressed at high levels in the kidney, but its physiological function in this organ is still unclear.
In this article, the researchers confirmed that FXR is generally distributed in the renal tubules. Treatment with FXR agonists can significantly reduce urine output and increase urine osmolality. FXR knockout mice showed impaired urine concentration, resulting in a polyuria phenotype. Furthermore, the researchers found that treatment of C57BL / 6 mice with chenodeoxycholic acid, an FXR endogenous ligand, can significantly upregulate the expression of renal aquaporin 2 (AQP2), while FXR gene defects can greatly reduce AQP2 in the kidney The expression level. In vitro studies have shown that the AQP2 gene promoter contains a FXR response element site, FXR can bind and activate this response element site, resulting in significantly increased AQP2 transcription in cultured primary medullary inner collecting duct cells.
These findings indicate that FXR plays a vital role in the regulation of urine volume. FXR activation can increase the concentration of urine by increasing the expression of the target gene AQP2 in the collecting duct.
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