Effect of Vitamin B2-Deficient Diet on Hydroxyproline- or Obesity-Induced Hyperoxaluria in Mice

Scope Hyperoxaluria is a major cause of kidney stone disease. Around half of the oxalate in mammals is supplied from the diet and the other half is endogenously synthesized from glyoxylate. Reduction of hepatic glycolate oxidase (GO) activity is one approach to reduce endogenous production of oxalate. However, there are currently few effective dietary approaches to reduce hepatic GO activity. Methods and Results In the present study, it is investigated whether restriction of dietary vitamin B2 (VB2) can reduce hepatic GO activity and oxalate excretion in mice with hyperoxaluria induce by hydroxyproline (Hyp) or obesity. It is found that VB2 restriction significantly reduces hepatic GO activity in both the Hyp- and obesity-induced model of hyperoxaluria in mice. However, VB2 restriction reduces urinary oxalate excretion only in the Hyp-treated mice and not the obese mice. This difference could be due to the contribution of endogenous oxalate production that manifests as increased hepatic GO activity in Hyp-treated mice but not obese mice. Conclusion Together these results suggest that VB2 restriction could be a new dietary approach to improve hyperoxaluria when endogenous production of oxalate is increased.

Automated summary

The study found that dietary restriction of vitamin B2 significantly reduces hepatic glycolate oxidase (GO) activity in mice with hyperoxaluria induced by hydroxyproline (Hyp) or obesity. Furthermore, this restriction only decreased urinary oxalate excretion in Hyp-treated mice and not in obese mice, possibly due to differences in endogenous oxalate production between the two groups. These results suggest that dietary vitamin B2 restriction could be a new approach to improve hyperoxaluria in conditions where endogenous oxalate production is increased.