Purpose: Urinary oxalate has an important role in the formation of calcium oxalate stone and approximately 50% to 60% of urinary oxalate is derived from the endogenous metabolism of glyoxylate. Glyoxylate is enzymatically converted to glycine by alanine-glyoxylate aminotransferase in the liver and vitamin B6 has a key role as a coenzyme. Therefore, we evaluated hepatic alanine-glyoxylate aminotransferase activity and oxalate metabolism in vitamin B6 deficient rats.
Materials and Methods: A total of 12 male Wistar rats were fed a control or a vitamin B6 deficient diet. After 4 weeks creatinine, oxalate, glycolate, glycine and citrate in the urine, and alanine-glyoxylate aminotransferase activity and its mRNA level in the liver were measured.
Results: Urinary oxalate-to-creatinine and glycolate-to-creatinine ratios were significantly higher in vitamin B6 deficient rats than in control rats but urinary glycine-to-creatinine and citrate-to-creatinine ratios were significantly lower. Hepatic alanine-glyoxylate aminotransferase activity and its mRNA level were significantly lower in vitamin B6 deficient rats than in control rats.
Conclusions: Vitamin B6 deficiency not only decreased alanine-glyoxylate aminotransferase activity, but also down-regulated alanine-glyoxylate aminotransferase gene expression by hepatocytes and led to hyperoxaluria and hyperglycolic aciduria secondary to impaired metabolism of oxalate precursors. Hyperoxaluria with hypocitruria may also contribute to calcium oxalate stone formation in vitamin B6 deficiency.