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  • Title: Hepatic cytochrome P-450j induction in the spontaneously diabetic BB rat.
    Author: Bellward GD, Chang T, Rodrigues B, McNeill JH, Maines S, Ryan DE, Levin W, Thomas PE.
    Journal: Mol Pharmacol; 1988 Feb; 33(2):140-3. PubMed ID: 3277033.
    Abstract:
    Hepatic microsomal cytochrome P-450j has been studied using the male spontaneously diabetic BB rat as a model for insulin-dependent diabetes. This approach avoids any direct hepatotoxic effects from chemical diabetogenic agents. Both diabetic rats maintained on insulin and nondiabetic littermates were used as controls. Levels of cytochrome P-450j were increased approximately 3-fold in the diabetics 4 days after the cessation of insulin therapy. In addition, cytochrome P-450j-catalyzed enzymatic activities, aniline hydroxylation, and N-nitrosodimethylamine N-demethylation were increased by the diabetic state at this same time period. Cytochrome P-450f remained at control levels in all groups of animals. In order to test the hypothesis that ketone bodies are involved in the increase in cytochrome P-450j in the diabetic state, plasma beta-hydroxybutyrate levels were monitored. Hepatic aniline hydroxylation, N-nitrosodimethylamine N-demethylation, and cytochrome P-450j levels in individual animals were found to correlate with plasma beta-hydroxybutyrate levels (r = 0.59-0.71 p less than 0.001). In contrast, no significant correlation between levels of cytochrome P-450j and plasma glucose, insulin, or cholesterol was observed in individual animals (r = 0.07-0.23, p greater than 0.4). We conclude that cytochrome P-450j is induced in the livers of spontaneously diabetic rats, and that this induction may be associated directly or indirectly with elevated plasma ketone levels.
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