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Related Experiment Videos

Ketogenesis in chick embryo isolated hepatocytes.

A J Bate, A J Dickson

    Comparative Biochemistry and Physiology. B, Comparative Biochemistry
    |January 1, 1984
    PubMed
    Summary

    Isolated chick embryo hepatocytes show high ketogenesis. Long-chain fatty acids stimulate this process, while glucose and certain metabolites inhibit it, with hormones having no effect.

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    Area of Science:

    • Biochemistry
    • Cell Biology
    • Developmental Biology

    Background:

    • Chick embryo hepatocytes possess high endogenous ketogenesis rates.
    • Understanding the regulation of ketogenesis in embryonic development is crucial.

    Purpose of the Study:

    • To investigate the factors influencing ketogenesis in isolated chick embryo hepatocytes.
    • To determine the effects of various fatty acids, metabolites, and hormones on ketogenesis.

    Main Methods:

    • Isolation of hepatocytes from 17-day chick embryos.
    • Incubation of hepatocytes with different substrates (fatty acids, glucose, propionate, pyruvate, lactate) and hormones (glucagon, insulin, adrenalin, vasopressin).
    • Measurement of ketogenesis rates under various conditions.

    Main Results:

    • Long-chain fatty acids (palmitate > oleate > stearate) significantly stimulated ketogenesis.
    • Octanoate showed a biphasic effect: stimulation at low concentrations and inhibition at high concentrations.
    • Glucose did not affect endogenous ketogenesis, while propionate, pyruvate, and lactate inhibited it.
    • Glucagon, insulin, adrenalin, and vasopressin did not alter ketogenesis rates.

    Conclusions:

    • Chick embryo hepatocytes are highly capable of ketogenesis.
    • Ketogenesis is modulated by specific fatty acids and metabolic intermediates.
    • Hormonal regulation of ketogenesis appears limited in this embryonic model.

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