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Induction of tyrosine aminotransferase in utero by anti-insulin agents

M H Cake

    The Biochemical Journal
    |September 15, 1986
    PubMed

    Insights

    The study shows that decreased insulin levels in newborn rats trigger the premature rise of tyrosine aminotransferase, a key liver enzyme. This suggests falling insulin at birth is crucial for enzyme development.

    Area of Science:

    • Biochemistry
    • Developmental Biology
    • Endocrinology

    Background:

    • The liver enzyme tyrosine aminotransferase (TAT) is typically low in fetal rats, increasing after birth.
    • Hormonal regulation of fetal development is critical for postnatal adaptation.

    Purpose of the Study:

    • To investigate the role of insulin in the postnatal induction of hepatic tyrosine aminotransferase.
    • To explore the mechanisms regulating TAT expression during late gestation and early postnatal life.

    Main Methods:

    • Induction of diabetes in pregnant rats using streptozotocin to alter fetal insulin levels.
    • Administration of anti-insulin serum to fetuses to artificially lower insulin concentrations.
    • Measurement of tyrosine aminotransferase activity in fetal and neonatal rat livers.

    Main Results:

    • Premature induction of TAT was observed in fetuses of diabetic rats (low insulin).
    • Artificial reduction of fetal insulin levels also led to precocious TAT induction.
    • These findings correlate reduced insulin with increased TAT activity.

    Conclusions:

    • Decreased plasma insulin concentration is a significant factor in the postnatal induction of tyrosine aminotransferase.
    • The natural decline in insulin around birth likely initiates the surge of TAT activity.
    • Insulin acts as a key regulator suppressing TAT during fetal development.

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