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Effect of Vitamin B2-Deficient Diet on Hydroxyproline- or Obesity-Induced Hyperoxaluria in Mice
Takashi Uebanso1, Mai Suyama1, Takaaki Shimohata1
1Department of Preventive Environment and Nutrition, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, 770-8503, Japan.
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.
Insights
Restricting dietary vitamin B2 (VB2) lowers liver glycolate oxidase (GO) activity, a key enzyme in oxalate production. This dietary change may help manage hyperoxaluria, particularly when endogenous oxalate synthesis is elevated.
Area of Science:
- Biochemistry
- Nutrition Science
- Nephrology
Background:
- Hyperoxaluria is a significant factor in kidney stone formation.
- Oxalate originates from both dietary intake and endogenous synthesis from glyoxylate.
- Reducing hepatic glycolate oxidase (GO) activity is a strategy to decrease endogenous oxalate production, but effective dietary methods are limited.
Purpose of the Study:
- To investigate if dietary vitamin B2 (VB2) restriction can decrease hepatic GO activity and oxalate excretion.
- To evaluate VB2 restriction in mouse models of hyperoxaluria induced by hydroxyproline (Hyp) or obesity.
Main Methods:
- Administered VB2 restriction to mice with Hyp- or obesity-induced hyperoxaluria.
- Measured hepatic GO activity and urinary oxalate excretion.
Main Results:
- VB2 restriction significantly reduced hepatic GO activity in both hyperoxaluric models.
- Urinary oxalate excretion decreased only in Hyp-treated mice, not obese mice.
- Observed differences suggest varying contributions of endogenous oxalate production in different hyperoxaluric models.
Conclusions:
- VB2 restriction shows potential as a dietary intervention for hyperoxaluria.
- This approach is most effective when increased endogenous oxalate production is a primary factor.
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