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Published on: October 30, 2015
Mitochondrial oxidative metabolism during respiratory infection in riboflavin deficient mice
S Brijlal1, A V Lakshmi, M S Bamji
1National Institute of Nutrition, Indian Council of Medical Research, Jamai Osmania, Hyderabad, India.
Abstract:
Studies in children and mice have shown that respiratory infection alters riboflavin metabolism, resulting in increased urinary loss of this vitamin. This could be due to mobilization of riboflavin from the liver to blood because liver Flavin adenine dinucleotide (FAD) levels were lowered in the mice during infection. To understand the functional implications of lowered hepatic FAD levels during respiratory infection, flavoprotein functions such as oxidative phosphorylation and beta-oxidation of the liver mitochondria were examined during infection in mice. Weanling mice were fed either riboflavin-restricted or control diet for 18 days and then injected with a sublethal dose of Klebsiella pneumoniae. During infection, the state 3 respiratory rate with palmitoyl-L-carnitine and glutamate were significantly lowered (27-29%) in the riboflavin-restricted group, whereas in the control group 10% reduction was observed with palmitoyl-L-carnitine as substrate. A 22% reduction in the respiratory control ratio with palmitoyl-L-carnitine as substrate was observed during infection in the riboflavin-restricted group. The beta-oxidation of palmitoyl-L-carnitine was significantly lowered (29%) in the riboflavin-restricted infected group. The results of the study suggest that the effects of infection on vital physiologic functions were more pronounced in the riboflavin-restricted mice than in the control mice.
Insights
Respiratory infections impair riboflavin metabolism, leading to increased vitamin loss. Riboflavin deficiency exacerbates infection
Area of Science:
- Biochemistry
- Nutritional Science
- Immunology
Background:
- Respiratory infections disrupt riboflavin metabolism, causing increased urinary riboflavin excretion.
- Reduced liver Flavin adenine dinucleotide (FAD) levels during infection suggest vitamin mobilization from the liver.
- Understanding the impact of low hepatic FAD on mitochondrial function during infection is crucial.
Purpose of the Study:
- To investigate the functional consequences of lowered hepatic FAD levels during respiratory infection.
- To examine the effects of infection on flavoprotein functions, specifically oxidative phosphorylation and beta-oxidation in liver mitochondria.
- To compare the impact of infection on these functions in riboflavin-restricted versus control mice.
Main Methods:
- Weanling mice were fed either a riboflavin-restricted or control diet for 18 days.
- Mice were subsequently injected with a sublethal dose of Klebsiella pneumoniae to induce respiratory infection.
- Mitochondrial functions, including state 3 respiratory rate and respiratory control ratio using specific substrates (palmitoyl-L-carnitine, glutamate), were assessed.
- Liver mitochondrial beta-oxidation rates were measured.
Main Results:
- Infection significantly lowered state 3 respiratory rate (27-29%) with palmitoyl-L-carnitine and glutamate in riboflavin-restricted mice.
- A 10% reduction in state 3 respiratory rate with palmitoyl-L-carnitine was noted in control infected mice.
- The respiratory control ratio decreased by 22% with palmitoyl-L-carnitine in infected riboflavin-restricted mice.
- Beta-oxidation of palmitoyl-L-carnitine was significantly reduced (29%) in infected riboflavin-restricted mice.
Conclusions:
- Respiratory infection exacerbates the negative effects of riboflavin deficiency on vital physiological functions.
- Lowered hepatic FAD levels during infection impair mitochondrial oxidative phosphorylation and beta-oxidation.
- Riboflavin status critically influences the host's ability to maintain metabolic function during respiratory infections.
