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E-hmss, D. S. M., AND ROSE, C. I. Impaired labelling of liver phosphatidylethanolamine from ethsmola~nine-~~C in choline deficiency. Can. J. Biochea. 48, 885-8921 (1970).Ethanolamine-"C was injected intraportally to eight rats after 3 days of choline-deficient (c.d.1 feeding and to eight choline-supplemented (c.s.) rats. The rats were killed in groups of two after 4, 8, 98, and 32 min. Much less 14C was incorporated into phosphatidylethanolamine and phosphatidylcholine in the c.d. livers, while the level of the former phospholipid was increased and the latter was decreased in these livers.The liver water-soluble constituents were separated by anion and cation exchange chromatography and the following components were analyzed: choline, ethanolamine, glyeerophosphocholine, glycerophosphoethanslamine, choline phosphate, ethanolamine phosphate, and GDP-ethanolamine. In c.d. liver the levels sf ethanolamine and its derivatives were increased while choline and choline phosphate were reduced. There was a lower incorporation of ethanolamine-I4C into CDP-ethmolamine in the deficient livers whereas the specific radioactivities of ethanolamine and ethanolamine phosphate were increased.These findings are interpreted as indicating the existence of a block at the CTP : ethanolamine phosphate transferase step of phosphatidylethanolamine synthesis in c.d. liver.

The changes in liver and plasma lipids in choline deficiency were studied in vivo and in vitro. In choline deficiency, after a lag period of several days, total liver lipids rose rapidly and a relatively small decrease of plasma triglycerides was noted at about the same time. In the recovery experiments, a significant increase of plasma phospholipids occurred within 24 hours after choline had been restored to the diet of the deficient animals.When livers from normal rats (choline-supplemented) were perfused with blood diluted with buffer, triglyceride was released to the perfusate. Livers from choline-deficient rats (perfused with blood from similar deficient rats) failed to make a net contribution of triglyceride to the perfusate. A moderate recovery of transport of triglyceride from liver to plasma occurred within 4 to 7 days after choline had been restored to the diet of rats that had been fed the deficient diet for 3 weeks. These studies provided firm support for the hypothesis that, in choline deficiency, transport of triglyceride from the liver is impaired.

bibs tractThe disturbance in lipid metabolism caused by deficiency of dietary choline ira rats was investigated with H"-pa%mitic acid as a tracer. The incorporation of radioactivity into blood triglycerides, as compared to that in chcsline-supplemented contrs8s, showed a striking decline in rats taken a t intervals during the development of &olirne deficiency. This was partially corrected by choline refeeding for 2 days and was normal after 4 days of choline re-feeding. Both the total amounts and the radioactivities of phosphatidyl choliile in the liver and total phospholipids in the plasma were reduced in ehsline deficiency and were restored by choline re-feeding, whereas phosphatidyl ethanolamine in the liver was not affected. The findings confirm that the fatty liver of choiine deficiency is the result of an impairment in the transport of triglyceride from the liver, and support the hypothesis that it occurs because of a restriction in the synthesis of phosghstidyl choline which is required for lipoprotein formation.-A marked reduction in the transformation of I4C-ethanolamine into phosphatidyl choline was evident in choline deficiency, but most of the increase in liver phosphatidyl choline which occurred subsequent to choline re-feeding appeared t o be from synthesis by the direct (CBP-cholinej pathway.

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