Dietary protein deficiency induced changes in protein kinase C activity and phospholipid metabolism in rat hepatocytes

Dietary protein deficiency is known to alter the protein kinase C activity in various tissues of rats. Protein kinase C activity is influenced by the metabolism of membrane phosphoinositides and phosphatidyl choline (PC). For metabolic studies, hepatocytes have been the cells of choice of various wo...

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Bibliographic Details
Published inIndian journal of experimental biology Vol. 35; no. 9; p. 972
Main Authors Kathayat, R, Jaiswal, A S, Basir, S F, Bansal, S K
Format Journal Article
LanguageEnglish
Published India 01.09.1997
Subjects
Animals
Liver - cytology
Liver - metabolism
Male
Phospholipids - metabolism
Protein Deficiency
Protein Kinase C - metabolism
Rats
Rats, Wistar
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Summary:Dietary protein deficiency is known to alter the protein kinase C activity in various tissues of rats. Protein kinase C activity is influenced by the metabolism of membrane phosphoinositides and phosphatidyl choline (PC). For metabolic studies, hepatocytes have been the cells of choice of various workers. Therefore, studies on protein kinase C and these phospholipids were conducted in hepatocytes of rats maintained on three different diets viz. casein (20% protein) deficient (4% protein, rice flour as source of protein) and supplemented (deficient diet supplemented with L-lysine and DL-threonine) diet for 28 days. The protein deficiency in diet led to a decline in protein kinase C activity (P < 0.01) without effecting its translocation, an increase in phosphatidyl inositol 4,5-bisphosphate (P < 0.001) and a decrease in phosphatidyl inositol 4-monophosphate and phosphatidyl inositol (P < 0.01) but did not alter the PC contents, as compared to the casein group. Supplementation of deficient diet with L-lysine and DL-threonine could considerably reverse the effect of deficiency of protein in diet. The results suggest that quality of dietary protein is mainly relevant for maintaining phospholipid metabolism and physiology of hepatocytes and thus the signalling mechanism in these cells.
ISSN:0019-5189