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Uric acid transport and disease
Alexander So, Bernard Thorens
Alexander So, Bernard Thorens
Published June 1, 2010
Citation Information: J Clin Invest. 2010;120(6):1791-1799. https://doi.org/10.1172/JCI42344.
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Science in Medicine Article has an altmetric score of 16

Uric acid transport and disease

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Abstract

Uric acid is the metabolic end product of purine metabolism in humans. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironment. Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. We discuss here the biology of urate metabolism and its role in disease. We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.

Authors

Alexander So, Bernard Thorens

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Figure 1

Pathways of urate homeostasis.

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Pathways of urate homeostasis.
Summary scheme of the pathways to produce...
Summary scheme of the pathways to produce uric acid, to convert it into allantoin by the liver enzyme uricase, and to excrete it. The balance between these pathways regulates blood urate concentrations, which are higher in humans and apes due to inactivation of the uricase genes. Hyperuricemia can lead to gout and possibly to cardiovascular effects, whereas hyperuricosuria may leads to uric acid crystal–induced pathologies.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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