A Rapid Effect of Thyroxine on Accumulation of Diacylglycerols and on Activation of Protein Kinase C in Liver Cells

N. S. Kavok¹, O. A. Krasil'nikova¹, O. M. Sidorkina², and N. A. Babenko^1*

¹Institute of Biology, Kharkov National University, pl. Svobody 4, Kharkov, 61077 Ukraine; fax: (0572) 35-2923; E-mail: babenko@univer.kharkov.ua

²Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, pr. Lavrent'eva 10, Novosibirsk, 630090 Russia; fax: (3832) 33-1278

^* To whom correspondence should be addressed.

Received March 23, 2000; Revision received August 2, 2000

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L-Thyroxine rapidly stimulated the accumulation of diacylglycerols in isolated hepatocytes and in liver when lipids were prelabeled with [¹⁴C]oleic acid or with [¹⁴C]CH₃COONa. Perfusion of the liver of hypothyroid animals with L-thyroxine-containing solution or incubation of liver fragments with the hormone increased the content of diacylglycerols in the liver cells. The increase in [¹⁴C]diacylglycerol level in the liver cells was accompanied by a decrease in the level of [¹⁴C]phosphatidylcholine, whereas contents of other ¹⁴C-labeled phospholipids, such as phosphatidylethanolamine, sphingomyelin, lysophosphatidylcholine, phosphatidylinositol (PtdIns), phosphatidylinositol-4-phosphate (PtdIns4P), and phosphatidylinositol-4,5-bis-phosphate (PtdIns(4,5)P₂), and of ¹⁴C-labeled fatty acids were the same as in the control. The L-thyroxine-induced accumulation of diacylglycerols in hepatocytes was not affected by neomycin but was inhibited by propranolol. Incubation of hepatocytes prelabeled with [¹⁴C]oleic acid with L-thyroxine and ethanol (300 mM) was accompanied by generation and accumulation of [¹⁴C]phosphatidylethanol that was partially suppressed by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). L-Thyroxine was responsible for the translocation of protein kinase C from the cytosol into the membrane fraction and for a many-fold activation of the membrane-bound enzyme. D-Thyroxine failed to affect the generation of diacylglycerols in hepatocytes and the activity of protein kinase C.

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KEY WORDS: liver, hepatocytes, thyroxine, diacylglycerols, phospholipase D, protein kinase C

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