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Related Experiment Videos

Pathophysiologic study on methylmalonic aciduria: decrease in liver high-energy phosphate after propionate loading in

A Nakai1, Y Shigematsu, M Saito

  • 1Department of Pediatrics, Fukui Medical School, Japan.

Pediatric Research
|July 1, 1991
PubMed
Summary

Vitamin B12 deficiency and propionate loading significantly deplete liver ATP levels in rats. Propionate also inhibits key enzymes in the tricarboxylic acid cycle, impacting cellular energy metabolism.

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Area of Science:

  • Biochemistry
  • Nutritional Science
  • Metabolic Research

Background:

  • Vitamin B12 deficiency impairs crucial metabolic pathways.
  • Propionate and methylmalonate are organic acids involved in metabolism.
  • Cellular energy status, particularly ATP levels, is vital for liver function.

Purpose of the Study:

  • To investigate the impact of vitamin B12 deficiency and organic acid loading on liver metabolism in rats.
  • To compare the effects of methylmalonate versus propionate infusion on ATP levels and metabolic intermediates.
  • To explore the potential inhibition of the tricarboxylic acid cycle by propionate.

Main Methods:

  • Intravenous infusion of methylmalonate or propionate into vitamin B12-deprived and control rats.
  • Measurement of plasma and liver vitamin B12 concentrations.

Related Experiment Videos

  • Analysis of liver propionate and methylmalonate levels.
  • 31P-magnetic resonance spectroscopy to assess the ratio of beta-ATP to inorganic phosphate.
  • Quantification of tricarboxylic acid cycle intermediates and related organic acids.

    • Main Results:

    • Vitamin B12-deprived rats showed significantly lower plasma and liver B12 concentrations.
    • Propionate loading led to a disproportionate increase in liver propionate levels.
    • Both methylmalonate and propionate loading decreased liver ATP levels, with propionate causing a more marked reduction.
    • Vitamin B12 deprivation exacerbated the decrease in ATP levels compared to control rats.
    • Elevated liver propionate and methylmalonate levels in B12-deprived rats suggest metabolic dysregulation.
    • Analysis of liver metabolites indicated that propionate likely inhibits NAD(+)-dependent enzymes in the tricarboxylic acid cycle.

    Conclusions:

    • Vitamin B12 deficiency and propionate loading significantly impair liver energy metabolism by reducing ATP levels.
    • Propionate appears to inhibit key enzymes within the tricarboxylic acid cycle, disrupting cellular respiration.
    • These findings highlight the critical role of vitamin B12 in maintaining metabolic homeostasis and the detrimental effects of propionate accumulation.