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Tissue distribution and turnover of [3H]riboflavin during respiratory infection in mice
1Department of Biochemistry, National Institute of Nutrition, Indian Council of Medical Research, Hyderabad.
Abstract:
Studies in children and mice suggest that respiratory infections cause a mobilization of riboflavin from the tissues to the blood, resulting in increased urinary loss of this vitamin. To verify this observation, the tissue distribution and turnover of [3H]riboflavin were investigated in control and low-riboflavin-fed mice infected with Klebsiella pneumoniae. Infection significantly reduced [3H]riboflavin levels in the liver and kidney of low-riboflavin-fed mice and in the liver of control mice. Such changes were not observed in tissues such as muscle, small intestine, and brain. Urinary excretion of [3H]riboflavin increased significantly during the acute phase of infection and the biological half-life of [3H]riboflavin was shorter in the low-riboflavin-fed group. The results confirm that the mobilization of riboflavin from tissues to blood during infection results in a deterioration of riboflavin status. Thus, the study supports the hypothesis that respiratory infection is a nondietary factor contributing to the high prevalence of subclinical riboflavin deficiency in children of developing countries like India.
Insights
Respiratory infections mobilize riboflavin from tissues, increasing urinary loss and worsening riboflavin status. This supports the link between infection and deficiency in children.
Area of Science:
- Biochemistry and Nutritional Science
- Infectious Disease Research
Background:
- Respiratory infections may alter vitamin metabolism.
- Previous studies suggest riboflavin (vitamin B2) is mobilized during infection, leading to increased urinary excretion.
Purpose of the Study:
- To investigate the effect of bacterial infection (Klebsiella pneumoniae) on riboflavin tissue distribution and turnover in mice.
- To confirm if infection-induced riboflavin mobilization contributes to subclinical deficiency.
Main Methods:
- Used radiolabeled [3H]riboflavin to track tissue distribution and biological half-life in control and low-riboflavin-fed mice.
- Infected mice with Klebsiella pneumoniae to simulate respiratory infection.
- Measured [3H]riboflavin levels in various tissues (liver, kidney, muscle, intestine, brain) and urine.
Main Results:
- Infection significantly decreased [3H]riboflavin levels in the liver and kidney of low-riboflavin mice, and in the liver of control mice.
- No significant changes were observed in muscle, small intestine, or brain riboflavin levels.
- Urinary excretion of [3H]riboflavin increased during infection, and its biological half-life was shorter in deficient mice.
Conclusions:
- Respiratory infection causes riboflavin to shift from tissues to the blood, leading to increased urinary loss.
- This mobilization results in a poorer riboflavin status, supporting the hypothesis that infection is a factor in subclinical riboflavin deficiency.
- Findings suggest a link between respiratory infections and the high prevalence of riboflavin deficiency in children in developing countries.
