Effects of inhibitors of diacylglycerol metabolism on protein kinase C-mediated responses in hepatocytes

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    Abstract

    In hepatocytes pre-labelled with [3H]glycerol, compound R59022 (6-[2-(4-[(4-fluorophenyl)phenylmethylenel-l-piperidinyl)ethyl-7-methyl-5H-thiazolo[3,2-alpyrimidin-5-one) and 2-bromooctanoate each increased the amount of radioactivity in diacylglycerols. R59022 mimicked the actions of 12-O-tetradecanoylphorbol 13-acetate in completely abolishing the activation by adrenaline (but not that by vasopressin or glucagon) of glycogen phosphorylase a, and in decreasing the activity of glycogen synthetase. Exogenous dioctanoylglycerol caused a small inhibition of adrenaline-stimulated phosphorylase activity. The concentration of R59022 which gave half-maximal inhibition of adrenaline-stimulated phosphorylase activity was 15 μM. Maximal inhibition was observed within 2 min of addition of R59022. 2-Bromooctanoate activated phosphorylase by a process independent of changes in cyclic AMP and Ca2+, and decreased glycogen synthetase. It is concluded that in hepatocytes (i) diacylglycerols which accumulate as a result of the inhibition of diacylglycerol kinase by R59022 activate protein kinase C and (ii) 2-bromooctanoate increases diacylglycerols but also has other effects on hepatocyte metabolism.

    Original languageEnglish
    Pages (from-to)68-74
    Number of pages7
    JournalBBA - Molecular Cell Research
    Volume970
    Issue number1
    DOIs
    Publication statusPublished - 8 Jun 1988

    Keywords

    • (Hepatocyte)
    • Diacylglycerol metabolism
    • Metabolic inhibitor
    • Protein kinase C

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