Actually, the intestinal cell-specific SLC2A9 gene knock-out mice had elevated serum urate levels, and the mice lacking the SLC2A9 gene were prone to metabolic syndrome (high uric acid, hypertension, hyperglycemia, hyperlipidemia), indicating that SLC2A9 mediates the excretion of uric acid from the intestine (43). This evidence concerns the gene SLC2A9 and hyperlipidemia.