scholarly journals Control of phosphatidylcholine synthesis and the regulatory role of choline kinase in rat liver. Evidence from essential-fatty acid-deficient rats

1978 ◽  
Vol 176 (2) ◽  
pp. 631-633 ◽  
Author(s):  
J P Infante ◽  
J E Kinsella

Choline kinase and phosphocholine cytidylytransferase catalyse the rate-limiting steps of the cytidine pathway for the synthesis of phosphatidylcholine [Infante (1977) Biochem. J. 167, 847–849]. Essential-fatty acid deficiency induces a 3.5-fold increase in the specific activity of choline kinase, whereas the specific activity of the cytidylytransferase remains unchanged in rat liver. This change in specific activity accounts for the calculated increase in flux through the cytidine pathway produced in vivo by the same dietary state [Trewhella & Collins (1973 Biochim. Biophys. Acta 296, 34–50], thus confirming the fact that choline kinase has a regulatory role in the cytidine pathway for the synthesis of phosphatidylcholine.

1979 ◽  
Vol 179 (3) ◽  
pp. 723-725 ◽  
Author(s):  
J P Infante ◽  
J E Kinsella

Essential-fatty acid deficiency produces a 52% increase in the rate of phosphatidyl-ethanolamine synthesis in rat liver as calculated from results obtained in vivo [Trewhella & Collins (1973) Biochem. Biophys. Acta 296, 34–50]. This flux change was used to test the possible regulatory roles of ethanolamine kinase and of phosphoethanolamine cytidylyltransferase, which are rate-limiting enzymes of the cytidine pathway for the synthesis of phosphatidylethanolamine [Infante (1977) Biochem. J. 167, 847–849]. The results show that essential-fatty acid deficiency produces 50% and 53% increases respectively in the specific activity of these enzymes, accounting for the increased rate of phosphatidylethanolamine synthesis produced by this dietary insufficiency. This evidence leads to the conclusion that ethanolamine kinase and phosphoethanolamine cytidylyl-transferase have co-ordinated regulatory roles in the flux control of the cytidine pathway, and its sphinganine 1-phosphate lyase branch reaction, for the synthesis of phosphatidylethanolamine.


1995 ◽  
Vol 268 (1) ◽  
pp. R164-R170 ◽  
Author(s):  
U. C. Kopp ◽  
D. M. Farley ◽  
L. A. Smith ◽  
H. R. Knapp

The role of prostaglandins in renal sensory receptor activation was examined in rats fed an essential fatty acid-deficient (EFAD) diet to cause tissue arachidonate depletion. Littermates fed a standard diet were used as controls. In anesthetized rats, the increases in afferent renal nerve activity due to increasing ureteral pressure 2.5, 5, 7.5, 10, 12.5, and 15 mmHg were significantly reduced by the EFAD diet (P < 0.02): 3 +/- 5, 3 +/- 5, 11 +/- 5, 9 +/- 5, 19 +/- 3, and 17 +/- 5%, respectively, in EFAD rats and 23 +/- 11, 36 +/- 15, 50 +/- 15, 52 +/- 8, 72 +/- 17, and 90 +/- 19%, respectively, in control rats. In EFAD rats, addition of prostaglandin E2 (PGE2) to the renal pelvic perfusate restored the afferent renal nerve activity response to increased ureteral pressure toward that in control rats. PGE2 had no effect in control rats. Also the afferent renal nerve activity responses to renal pelvic perfusion with bradykinin at 4, 20, 100, and 500 micrograms/ml were significantly suppressed by the EFAD diet (P < 0.01): 13 +/- 15, 5 +/- 7, 60 +/- 19, and 63 +/- 20%, respectively, in EFAD rats and 122 +/- 23, 142 +/- 31, 172 +/- 19, and 190 +/- 39%, respectively, in control rats. These results demonstrate an important role for arachidonate metabolites, particularly PGE2, in renal sensory receptor activation. Together with our previous studies showing that indomethacin blocks the afferent renal nerve activity responses to increased ureteral pressure or bradykinin, the present studies provide strong evidence for an essential role of prostaglandins in renal sensory receptor activation.


Lipids ◽  
1994 ◽  
Vol 29 (3) ◽  
pp. 151-155 ◽  
Author(s):  
Leslie G. Cleland ◽  
Michael J. James ◽  
Susanna M. Proudman ◽  
Mark A. Neumann ◽  
Robert A. Gibson

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