THE EFFECTS OF CHOLINE DEFICIENCY AND CHOLINE RE-FEEDING UPON THE METABOLISM OF PLASMA AND LIVER LIPIDS

1966 ◽  
Vol 44 (1) ◽  
pp. 45-57 ◽  
Author(s):  
D. S. M. Haines

The disturbance in lipid metabolism caused by deficiency of dietary choline in rats was investigated with H3-palmitic acid as a tracer. The incorporation of radioactivity into blood triglycerides, as compared to that in choline-supplemented controls, showed a striking decline in rats taken at intervals during the development of choline deficiency. This was partially corrected by choline re-feeding for 2 days and was normal after 4 days of choline re-feeding. Both the total amounts and the radioactivities of phosphatidyl choline in the liver and total phospholipids in the plasma were reduced in choline 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 choline 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 phosphatidyl choline which is required for lipoprotein formation.A marked reduction in the transformation of14C-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 to be from synthesis by the direct (CDP-choline) pathway.

1979 ◽  
Vol 57 (6) ◽  
pp. 566-572 ◽  
Author(s):  
S. Tokmakjian ◽  
D. S. M. Haines

The effect of dietary choline upon liver ethanolamine metabolism was investigated by measurement of the changes in the liver levels of phospholipids and their precursors and in the metabolism of intraportally administered [14C]ethanolamine which occur when choline feeding is restored to 3-day choline deficient rats. The earliest detectable actions of choline were restoration of the decreased liver phosphatidyl choline level and beginning decreases in the elevated levels of liver ethanolamine, ethanolamine phosphate, CDP-ethanolamine, and phosphatidyl ethanolamine. The impairment at the CTP:ethanolaminephosphate cytidylyltransferase (EC 2.7.7.14) reaction induced by choline deficiency was reversed more slowly than were the increased levels of the ethanolamine-containing intermediates.In a further experiment it was observed that the liver levels of all of the ethanolamine-containing compounds were progressively diminished when the content of dietary choline was increased up to 1.2%. These findings indicate that exogenous choline exerts an effect upon liver metabolism which causes decreases in the liver levels of ethanolamine and its derivatives, including phosphatidyl ethanolamine. The nature of this action of choline is not known. In an experiment where rats were fed a diet containing 1% ethanolamine, the pattern of increase in the levels of the liver ethanolamine-containing substances did not mirror the pattern found in choline deficiency. This suggests that the increases in liver ethanolamine compounds caused by dietary choline deficiency are not due primarily to an excessive accumulation of free ethanolamine.


1957 ◽  
Vol 35 (1) ◽  
pp. 845-852 ◽  
Author(s):  
Bruno Rosenfeld ◽  
Jessie M. Lang

Albino rats weighing 180–200 g. were fed diets containing 5, 9, and 19% protein. The influence of these diets, both with and without additional choline, on the level of serum phospholipid was measured and it was found that only in the presence of dietary choline, an increase of the protein content of the diet caused an elevation of the level of phospholipid in the serum. Measurement of the effect of the interval after feeding showed a significant decrease of serum phospholipid 16 hours after the removal of the choline-containing food. In choline deficiency no such effect was found. Measurement of the influence of duration of choline deficiency on the level of phospholipid in serum revealed an immediate fall to a lower level at the onset of the deficiency. This change was complete before a significant rise of the level of total liver lipids was apparent.


1969 ◽  
Vol 36 (3) ◽  
pp. 393-398 ◽  
Author(s):  
R. C. Noble ◽  
W. Steele ◽  
J. H. Moore

SummaryCows were given either a low-fat concentrate mixture or a concentrate mixture that contained 5 or 10% ‘stearic acid’ (85% pure) or 10% ‘palmitic acid’ (85% pure). The concentrate mixtures were given with a high roughage diet that supplied 4·4 kg of hay and 2·7 kg of sugar-beet pulp/day. Blood samples were taken from the cows on each dietary treatment and the plasma phospholipids were analysed.Phosphatidyl choline accounted for 70% of the plasma phospholipids when the cows were given the low-fat diet and about 86% of the plasma phospholipids when the cows were given the diets supplemented with the fatty acids. The inclusion of the fatty acids in the concentrate mixtures decreased the relative proportions of the plasma phosphatidyl ethanolamine, sphingomyelin and lysophosphatidyl choline but the relative proportion of the plasma phosphatidyl serine remained unchanged.When the diet was supplemented with stearic acid the concentrations of 18:0 and 16:0 in the phosphatidyl choline were unaltered but the concentration of 18:1 was increased and the concentration of 18:2 was decreased. When the diet was supplemented with palmitic acid the concentrations of 16:0 and 18:1 in the phosphatidyl choline were increased and the concentrations of 18:0 and 18:2 were decreased. In contrast, the inclusion of stearic acid in the diet increased the concentration of 18:0 in the phosphatidyl serine and decreased the concentration of 16:0; the concentrations of 18:1 and 18:2 were unchanged. The fatty acid composition of the plasma phosphatidyl ethanolamine was unaffected by dietary treatment. The effects of diet on the fatty acid compositions of the phosphatidyl choline and lysophosphatidyl choline were similar. Supplementation of the diet with stearic acid increased the concentrations of 18:0 and 18:1 in the plasma sphingomyelin and decreased the concentrations of 16:0 and 18:2. The addition of palmitic acid to the diet increased the concentration of 16:0 in the sphingomyelin but it decreased the concentrations of the other constituent fatty acids.


2011 ◽  
Vol 32 (6) ◽  
pp. 571-577 ◽  
Author(s):  
Han-Sol Park ◽  
Byeong Hwan Jeon ◽  
Sung Hoon Woo ◽  
Jaechan Leem ◽  
Jung Eun Jang ◽  
...  

1957 ◽  
Vol 35 (10) ◽  
pp. 845-852 ◽  
Author(s):  
Bruno Rosenfeld ◽  
Jessie M. Lang

Albino rats weighing 180–200 g. were fed diets containing 5, 9, and 19% protein. The influence of these diets, both with and without additional choline, on the level of serum phospholipid was measured and it was found that only in the presence of dietary choline, an increase of the protein content of the diet caused an elevation of the level of phospholipid in the serum. Measurement of the effect of the interval after feeding showed a significant decrease of serum phospholipid 16 hours after the removal of the choline-containing food. In choline deficiency no such effect was found. Measurement of the influence of duration of choline deficiency on the level of phospholipid in serum revealed an immediate fall to a lower level at the onset of the deficiency. This change was complete before a significant rise of the level of total liver lipids was apparent.


1968 ◽  
Vol 46 (3) ◽  
pp. 487-494 ◽  
Author(s):  
J. Blumenstein

The incorporation of metabolic precursors of lipids was followed in the livers of rats fed a semisynthetic diet supplemented with, or deficient in, choline. In the early stages of choline deficiency no change was observed in the net incorporation of palmitic acid into liver lipids. Experiments with labelled ethanolamine, choline, and methionine showed that during choline deficiency the direct incorporation of choline into liver lecithins is unchanged, whereas the incorporation of the methyl group of methionine into lecithin, and ethanolamine into cephalins is decreased.


1976 ◽  
Vol 29 (6) ◽  
pp. 419 ◽  
Author(s):  
Judith A Pearson ◽  
AR Johnson ◽  
RL Hood ◽  
AC Fogerty

Fatty liver and kidney syndrome, a disorder of young chicks, was studied under laboratory conditions. Affected chicks had enlarged livers (hepatomegaly), an increased content of lipid in the liver, and an increased level of palmitoleic acid in the liver lipids. The disorder was observed mainly in chicks from young parent flocks, and was associated either with commercial diets which were subsequently found to be low in biotin, or with specially formulated low-biotin diets. A third factor, imposition of stress, was required to initiate the disorder. There was evidence of increased lipogenesis causing an increase of triacylglycerols in the liver lipids and an increased production of saturated fatty acids, particularly palmitic acid. Increased levels of palmitoleic acid resulted from an increased desaturation of palmitic acid. Under stress, affected chicks had low blood glucose levels, suggesting that gluconeogenesis was impaired. Since biotin-dependent enzymes are involved in both gluconeogenesis and lipogenesis, it would appear that the relevant enzymes respond differently to a deficiency of biotin.


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