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尿酸转运与疾病。

Uric acid transport and disease.

机构信息

Service de Rhumatologie, Department of Musculoskeletal Medicine, University of Lausanne, Lausanne, Switzerland.

出版信息

J Clin Invest. 2010 Jun;120(6):1791-9. doi: 10.1172/JCI42344. Epub 2010 Jun 1.

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.

摘要

尿酸是人类嘌呤代谢的代谢终产物。它具有抗氧化特性,可能具有保护作用,但也可能具有促氧化作用,具体取决于其化学微环境。高尿酸血症通过形成尿酸盐晶体导致痛风而导致疾病易感性,但高尿酸血症,不依赖于晶体形成,也与高血压、动脉粥样硬化、胰岛素抵抗和糖尿病有关。我们在这里讨论尿酸代谢的生物学及其在疾病中的作用。我们还涵盖了尿酸转运的遗传学,包括 URAT1,以及最近的研究确定 SLC2A9(编码葡萄糖转运蛋白家族同工型 Glut9)作为血浆尿酸水平和痛风发展的主要决定因素。

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