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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Category: Science in Medicine

Uric acid transport and disease

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 4

Summary of Glut9 sites of expression and function.

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Summary of Glut9 sites of expression and function. Glut9 plays an import...
Glut9 plays an important role in the control of urate homeostasis by its role in several organs. In kidney, evidence strongly supports a major role of Glut9 in uric acid reabsorption; in intestine, Glut9 may participate in uric acid excretion, although there has been no direct testing of this hypothesis; in the liver of animals with active uricase, Glut9 is required for hepatic uric acid uptake and conversion to allantoin for excretion. Absence of uricase in humans raises the question of the role of hepatic Glut9 in humans. There is good evidence for Glut9 expression in chondrocytes and leukocytes, but so far there is no indication whether this transporter is required for uptake or secretion.