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Elevated intramitochondrial adenine nucleotides and mitochondrial function.

H C Hamman, R C Haynes

    Archives of Biochemistry and Biophysics
    |May 1, 1983
    PubMed
    Summary
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    Glucagon increases mitochondrial adenine nucleotides, but this does not directly enhance mitochondrial function. Loading mitochondria with nucleotides also failed to consistently improve specific metabolic processes.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Metabolic Regulation

    Background:

    • Glucagon administration to rats elevates hepatic mitochondrial adenine nucleotide content.
    • This increase is hypothesized to enhance mitochondrial function by facilitating adenine nucleotide transport across the inner mitochondrial membrane.

    Purpose of the Study:

    • To investigate the functional consequences of increased mitochondrial adenine nucleotide pools.
    • To test the hypothesis that an enlarged nucleotide pool directly stimulates mitochondrial bioenergetic functions.

    Main Methods:

    • In vitro loading of rat liver mitochondria with adenine nucleotides to supranormal levels.
    • Assay of mitochondrial functions including pyruvate carboxylation, uncoupler-dependent ATPase, and succinic dehydrogenase activity.

    Related Experiment Videos

  • Analysis of adenine nucleotide exchange rates and atractyloside sensitivity.

    • Main Results:

    • Mitochondrial loading stimulated pyruvate carboxylation, uncoupler-dependent ATPase, and succinic dehydrogenase activity, but not citrulline formation.
    • A sham loading procedure, without increasing nucleotide content, yielded similar stimulatory effects.
    • Enlarged nucleotide pools increased exchangeable nucleotides but did not significantly increase the rate of exchange.
    • Mitochondria from glucagon-treated rats showed no increased exchange rate despite an enlarged pool.
    • No correlation was found between nucleotide exchange rate and uncoupler-dependent ATPase activity.

    Conclusions:

    • The observed stimulation of mitochondrial functions by glucagon or in vitro loading is not solely attributable to an enlarged adenine nucleotide pool.
    • The rate of adenine nucleotide exchange across the inner mitochondrial membrane does not appear to be the rate-limiting factor for these functions.
    • Further investigation is needed to elucidate the precise mechanisms by which glucagon influences hepatic mitochondrial function.