The influence of dietary choline intake upon liver ethanolamine metabolism

1979 ◽  
Vol 57 (6) ◽  
pp. 566-572 ◽  
Author(s):  
S. Tokmakjian ◽  
D. S. M. Haines
Keyword(s):  
Phosphatidyl Choline ◽  
Phosphatidyl Ethanolamine ◽  
Liver Metabolism ◽  
Choline Deficiency ◽  
Choline Intake ◽  
Ethanolamine Phosphate ◽  
Dietary Choline ◽  
Excessive Accumulation

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.

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
Keyword(s):  
Lipid Metabolism ◽  
Fatty Liver ◽  
Palmitic Acid ◽  
Phosphatidyl Choline ◽  
Marked Reduction ◽  
Phosphatidyl Ethanolamine ◽  
Choline Deficiency ◽  
Liver Lipids ◽  
Dietary Choline ◽  
Plasma And Liver Lipids

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.

Dietary Choline Intake during Pregnancy and PEMT rs7946 Polymorphism on Risk of Preterm Birth: A Case-Control Study

2021 ◽  
pp. 1-10
Author(s):  
Jie Zhu ◽  
Yu-Hong Liu ◽  
Xiang-Long He ◽  
Martin Kohlmeier ◽  
Li-Li Zhou ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Case Control Study ◽  
Chinese Women ◽  
Case Control ◽  
Han Chinese ◽  
Food Frequency ◽  
Term Delivery ◽  
Choline Intake ◽  
Dietary Choline ◽  
Control Study

<b><i>Introduction and Aims:</i></b> Choline-metabolizing genetic variation may interact with choline intake on fetal programming and pregnancy outcome. This case-control study aims to explore the association of maternal choline consumption and phosphatidylethanolamine N-methyltransferase (PEMT) gene polymorphism rs7946 with preterm birth risk. <b><i>Methods:</i></b> 145 Han Chinese women with preterm delivery and 157 Han Chinese women with term delivery were recruited in Shanghai. Dietary choline intake during pregnancy was assessed using a validated food frequency questionnaire. Additionally, DNA samples were genotyped for PEMT rs7946 (G5465A) with plasma homocysteine (Hcy) levels measured. <b><i>Results:</i></b> Compared with the lowest quartile of choline intake, women within the highest consumption quartile had adjusted odds ratio (aOR) for preterm birth of 0.48 (95% confidence interval, CI [0.24, 0.95]). There was a significant interaction between maternal choline intake and PEMT rs7946 (<i>p</i> for interaction = 0.04), where the AA genotype carriers who consumed the energy-adjusted choline &#x3c;255.01 mg/day had aOR for preterm birth of 3.75 (95% CI [1.24, 11.35]), compared to those with GG genotype and choline intake &#x3e;255.01 mg/day during pregnancy. Additionally, the greatest elevated plasma Hcy was found in the cases with AA genotype and choline consumption &#x3c;255.01 mg/day (<i>p</i> &#x3c; 0.001). <b><i>Conclusion:</i></b> The AA genotype of PEMT rs7946 may be associated with increased preterm birth in these Han Chinese women with low choline intake during pregnancy.

Low dietary choline intake is associated with osteoporosis in elderly individuals: a population-based study

2021 ◽  
Author(s):  
Yuan-Wei Zhang ◽  
Pan-Pan Lu ◽  
Ying-Juan Li ◽  
Guang-Chun Dai ◽  
Mu-Min Cao ◽  
...  
Keyword(s):  
Bone Health ◽  
The Elderly ◽  
Population Based ◽  
Population Based Study ◽  
Elderly Individuals ◽  
Choline Intake ◽  
Dietary Choline ◽  
As If

Currently, little is known regarding the association between dietary choline intake and osteoporosis in the elderly individuals, as well as if such intakes affect bone health and result in fractures....

scholarly journals Dietary Choline Intake: Current State of Knowledge Across the Life Cycle

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1513 ◽  
Author(s):  
Alejandra Wiedeman ◽  
Susan Barr ◽  
Timothy Green ◽  
Zhaoming Xu ◽  
Sheila Innis ◽  
...  
Keyword(s):  
Life Cycle ◽  
Current Knowledge ◽  
Water Soluble ◽  
Food Sources ◽  
Soluble Form ◽  
Dietary Recommendations ◽  
Current State ◽  
Dietary Nutrient ◽  
Choline Intake ◽  
Dietary Choline

Choline, an essential dietary nutrient for humans, is required for the synthesis of the neurotransmitter, acetylcholine, the methyl group donor, betaine, and phospholipids; and therefore, choline is involved in a broad range of critical physiological functions across all stages of the life cycle. The current dietary recommendations for choline have been established as Adequate Intakes (AIs) for total choline; however, dietary choline is present in multiple different forms that are both water-soluble (e.g., free choline, phosphocholine, and glycerophosphocholine) and lipid-soluble (e.g., phosphatidylcholine and sphingomyelin). Interestingly, the different dietary choline forms consumed during infancy differ from those in adulthood. This can be explained by the primary food source, where the majority of choline present in human milk is in the water-soluble form, versus lipid-soluble forms for foods consumed later on. This review summarizes the current knowledge on dietary recommendations and assessment methods, and dietary choline intake from food sources across the life cycle.

scholarly journals Plasma Choline Concentration and Dietary Choline Intake of Some Korean Young Adults

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Young‐Jin Chung ◽  
Hyo‐Jung Cho ◽  
Jin‐Seok Na
Keyword(s):  
Young Adults ◽  
Choline Intake ◽  
Dietary Choline

scholarly journals LECITHIN SYNTHESIS, INTRACELLULAR TRANSPORT, AND SECRETION IN RAT LIVER

1969 ◽  
Vol 40 (2) ◽  
pp. 461-483 ◽  
Author(s):  
Olga Stein ◽  
Yechezkiel Stein
Keyword(s):  
Endoplasmic Reticulum ◽  
Liver Cell ◽  
Phosphatidyl Choline ◽  
Intracellular Transport ◽  
Phosphatidyl Ethanolamine ◽  
Specific Activity ◽  
Perfused Liver ◽  
Precursor Pool

Injection of choline-3H into choline-deficient rats resulted in an enhanced incorporation of the label into liver lecithin, as compared to the incorporation of label into liver lecithin of normal rats. The results obtained with the use of different lecithin precursors indicate that in the intact liver cell, both in vivo and in vitro, exchange of choline with phosphatidyl-choline is not significant. The synthesis and secretion of lecithins by the choline-deficient liver compare favorably with the liver of choline-supplemented rats, when both are presented with labeled choline or lysolecithin as lecithin precursors. Radioautography of the choline-deficient liver shows that 5 min after injection of choline-3H the newly synthesized lecithin is found in the endoplasmic reticulum (62%), mitochondria (13%), and at the "cell boundary" (20%). The ratio of the specific activity of microsomal and mitochondrial lecithin, labeled with choline, glycerol, or linoleate, was 1.53 at 5 min after injection, but the ratio of the specific activity of phosphatidyl ethanolamine (PE), labeled with ethanolamine, was 5.3. These results indicate that lecithin and PE are synthesized mainly in the endoplasmic reticulum, and are transferred into mitochondria at different rates. The site of a precursor pool of bile lecithin was studied in the intact rat and in the perfused liver. Following labeling with choline-3H, microsomal lecithin isolated from perfused liver had a specific activity lower than that of bile lecithin, but the specific activity of microsomal linoleyl lecithin was comparable to that of bile lecithin between 30 and 90 min of perfusion. It is proposed that the site of the bile lecithin pool is located in the endoplasmic reticulum and that the pool consists mostly of linoleyl lecithin.

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