Washington: A new animal study has revealed that excess uric acid in the blood might be the new culprit that disrupts normal metabolism.
The new research by Washington University School of Medicine in St. Louis suggested that the uric acid might play a role in causing metabolic syndrome, a cluster of risk factors that increases the risk of heart disease and type 2 diabetes.
Brian J. DeBosch, MD, said the gut was an important clearance mechanism for uric acid, opening the door to new potential therapies for preventing or treating type 2 diabetes and metabolic syndrome.
Recent research by the paper's senior author, Kelle H. Moley, MD, the James P. Crane Professor of Obstetrics and Gynecology, and her collaborators has shown that a protein called GLUT9 was an important transporter of uric acid.
The researchers also found that the drug allopurinol, which reduces uric acid production in the body and has long been used to treat gout, improved some, but not all, of the measures of metabolic health. Treatment with the drug lowered blood pressure and total cholesterol levels.
Exposure to uric acid would be impossible to avoid because it was a normal byproduct of cell turnover in the body. But there has been evidence that diet might contribute to uric acid levels. Many foods contain compounds called purines that break down into uric acid. And adding to growing concerns about fructose in the diet, evidence suggested that fructose metabolism in the liver also drives uric acid production.
The study is published in Nature Communications.
