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[Evolution of liver and kidney gluconeogenesis during acute liver intoxication by carbon tetrachloride (author's

P Hortelano, M J Faus, P Morata

    Revista Espanola De Fisiologia
    |September 1, 1979
    PubMed

    Insights

    Early kidney adaptation involves increased gluconeogenic capacity to compensate for liver damage from carbon tetrachloride. This metabolic shift in the kidney cortex helps maintain glucose homeostasis following liver intoxication.

    Area of Science:

    • Biochemistry
    • Toxicology
    • Physiology

    Context:

    • Investigates the metabolic response of rat kidneys to acute liver injury induced by carbon tetrachloride.
    • Examines the early adaptive changes in renal gluconeogenesis following toxic insult.

    Purpose:

    • To elucidate the role of renal metabolic adaptation in response to carbon tetrachloride-induced liver intoxication.
    • To understand the functional significance of enhanced kidney gluconeogenic capacity during early stages of liver impairment.

    Summary:

    • Carbon tetrachloride rapidly depletes liver glycogen and inhibits liver gluconeogenic capacity.
    • Kidney cortex exhibits enhanced phosphoenolpyruvate carboxykinase activity and gluconeogenic capacity.
    • Increased renal concentrations of key metabolites suggest accelerated gluconeogenesis in vivo, compensating for liver dysfunction.

    Impact:

    • Highlights the critical role of kidney cortex metabolic adaptation in maintaining homeostasis during early liver injury.
    • Provides insights into the compensatory mechanisms of the kidney in response to hepatotoxicity.
    • Suggests the kidney plays a vital role in mitigating the systemic effects of acute liver damage.

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