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Glucoregulation in acute liver failure.

H Vilstrup, J Iversen, N Tygstrup

    European Journal of Clinical Investigation
    |June 1, 1986
    PubMed
    Summary
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    Patients with acute liver failure showed significantly reduced glucose metabolism and insulin sensitivity, despite high insulin levels. Pancreatic hypersecretion of insulin and glucagon contributed to these metabolic disturbances.

    Area of Science:

    • Endocrinology
    • Metabolic Disorders
    • Hepatology

    Background:

    • Acute liver failure (ALF) presents complex metabolic challenges.
    • Patients with ALF often exhibit altered glucose homeostasis.
    • Understanding these alterations is crucial for managing ALF.

    Purpose of the Study:

    • To investigate glucose metabolism and insulin sensitivity in patients with fatal acute liver failure.
    • To characterize the hormonal milieu, specifically insulin and glucagon levels, in ALF.

    Main Methods:

    • Utilized the hyper- and euglycaemic glucose clamp technique in five ALF patients.
    • Measured plasma glucose, insulin, C-peptide, and glucagon concentrations.
    • Compared findings to reported control values.

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    Main Results:

    • Patients exhibited normal initial blood glucose but tenfold increased plasma insulin and C-peptide.
    • Whole-body glucose metabolic rate was halved, and insulin sensitivity decreased to 15% of control values.
    • Glucagon concentrations were fifty-fold increased and unresponsive to glucose and insulin, indicating pancreatic hypersecretion.

    Conclusions:

    • Patients with fatal ALF demonstrated profound insulin insensitivity and hyperinsulinaemia, primarily due to pancreatic hypersecretion.
    • The observed metabolic derangements highlight significant dysregulation of glucose metabolism in ALF.
    • The precise pathogenetic role and interrelation of these hormonal and metabolic findings in ALF require further investigation.