Abstract
Betaine as a dietary alkaloid has attracted the attention of patients with kidney
diseases. This study aimed to investigate the effects of betaine on serum uric acid
levels and kidney function, and explore their underlying mechanisms in potassium oxonate-induced
hyperuricemic mice. Betaine at 5, 10, 20, and 40 mg/kg was orally administered to
hyperuricemic mice for 7 days and found to significantly reduce serum uric acid levels
and increase fractional excretion of uric acid in hyperuricemic mice in a dose-dependent
manner. It effectively restored renal protein level alterations of urate transport-related
molecular proteins urate transporter 1, glucose transporter 9, organic anion transporter
1, and ATP-binding cassette subfamily G member 2 in this model, possibly resulting
in the enhancement of kidney urate excretion. Moreover, betaine reduced serum creatinine
and blood urea nitrogen levels and affected urinary levels of beta-2-microglobulin
and
N-acetyl-beta-D-glucosaminidase as well as upregulated renal protein levels of organic
cation/carnitine transporters OCT1, OCTN1, and OCTN2, resulting in kidney function
improvement in hyperuricemic mice. The findings from this study provide evidence that
betaine has anti-hyperuricemic and nephroprotective actions by regulating protein
levels of these renal organic ion transporters in hyperuricemic mice.
Key words
betaine - hyperuricemic mice - renal function - renal organic ion transporters