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Uric acid transport and disease.
Alexander So1, Bernard Thorens
1Service de Rhumatologie, Department of Musculoskeletal Medicine, University of Lausanne, Lausanne, Switzerland.
The Journal of Clinical Investigation
|June 3, 2010
Summary
High uric acid (hyperuricemia) can cause gout and is linked to other diseases. Genetics, including SLC2A9, significantly influence uric acid levels and gout risk.
Area of Science:
- Biochemistry and Human Metabolism
- Genetics of Renal Transport
Background:
- Uric acid is the primary end product of purine metabolism in humans.
- While possessing antioxidant properties, uric acid can also act as a pro-oxidant.
- Elevated uric acid levels (hyperuricemia) are associated with gout and other conditions like hypertension, atherosclerosis, insulin resistance, and diabetes, independent of crystal formation.
Purpose of the Study:
- To review the biological pathways of urate metabolism.
- To explore the role of uric acid in various human diseases.
- To discuss the genetic factors influencing urate transport and plasma levels.
Main Methods:
- Review of existing literature on urate metabolism and its clinical implications.
- Discussion of genetic studies focusing on urate transporters.
- Analysis of the role of URAT1 and SLC2A9 (Glut9) in uric acid homeostasis.
Main Results:
- Hyperuricemia is a significant risk factor for gout via urate crystal deposition.
- Independent of crystal formation, hyperuricemia is implicated in cardiovascular and metabolic diseases.
- Genetic variations in urate transporters, particularly SLC2A9 (Glut9), are major determinants of plasma uric acid levels and gout susceptibility.
Conclusions:
- Urate metabolism and transport are critical for maintaining health.
- Understanding the genetic basis of urate transport offers insights into disease predisposition.
- Targeting urate pathways may provide therapeutic strategies for metabolic and cardiovascular diseases.
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