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Public studies on ingredients:
Animal Study, Bacterial, Human In Vitro, Human Study, In Vitro Study.

Research & Studies:

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There are 39 good studies at Choline. Here's a selection:
Abstracts with Choline - Phosphatidylcholine Research

Epigenetic changes of the thioredoxin system in the tx-j mouse model and in patients with Wilson disease

Charles E Mordaunt Noreene M Shibata Dorothy A Kieffer Anna CzłonkowskaTomasz Litwin Karl H Weiss Daniel N Gotthardt Kristin Olson Dongguang WeiStewart Cooper ... Show more
Human Molecular Genetics, ddy262,
Published: 16 July 2018

Wilson disease (WD) is caused by mutations in the copper transporter ATP7B, leading to copper accumulation in the liver and brain. Excess copper inhibits S-adenosyl-L-homocysteine hydrolase, leading to variable WD phenotypes from widespread alterations in DNA methylation and gene expression. Previously, we demonstrated that maternal choline supplementation in the Jackson toxic milk (tx-j) mouse model of WD corrected higher thioredoxin 1 transcript levels in fetal liver. Here, we investigated the effect of maternal choline supplementation on genome-wide DNA methylation patterns in tx-j fetal liver by whole-genome bisulfite sequencing (WGBS). Tx-j Atp7b genotype-dependent differences in DNA methylation were corrected by choline for genes including, but not exclusive to, oxidative stress pathways. To examine phenotypic effects of postnatal choline supplementation, tx-j mice were randomized to one of six treatment groups: with or without maternal and/or continued choline supplementation, and with or without copper chelation with penicillamine (PCA) treatment. Hepatic transcript levels of thioredoxin 1 and peroxiredoxin 1 were significantly higher in mice receiving maternal and continued choline with or without PCA treatment compared to untreated mice. A WGBS comparison of human WD liver and tx-j mouse liver demonstrated a significant overlap of differentially-methylated genes associated with ATP7B deficiency. Further, eight genes in the thioredoxin pathway were differentially methylated in human WD liver samples. In summary, Atp7b deficiency and choline supplementation have a genome-wide impact, including on thioredoxin system-related genes, in tx-j mice. These findings could explain the variability of WD phenotype and suggest new complementary treatment options for WD.

Topic: oxidative stress - phenotype - homocysteine - gene expression - mutation - 
choline - dna methylation - etus - genes - genome - genotype - hepatolenticular -degeneration - hydrolase - membrane transport proteins - milk - mothers -
penicillamine - thioredoxin - brain - copper - liver - mice - epigenetics - 
copper chelation therapy
Phospholids protect the pancreas against alchohol-induced oxidative stress.
Abstract Source:
Free Radic Biol Med. 1999 Mar;26(5-6):609-19. PMID: 10218649
Abstract Author(s):
S I Aleynik, M A Leo, M K Aleynik, C S Lieber
Article Affiliation:
Section of Liver Disease&Nutrition and Alcohol Research Center, Bronx VA Medical Center and Mt. Sinai School of Medicine, New York, NY 10468, USA.
Oxidative stress is considered to be a forerunner of pancreatitis. Since we had found polyenylphosphatidylcholine, a mixture of polyunsaturated phosphatidylcholines extracted from soybeans, to protect against hepatic oxidative stress, we now tested its effects on the pancreas. Sprague-Dawley rats were pair-fed for two months nutritionally adequate liquid diet containing ethanol (36% of energy) or isocaloric carbohydrate, with either polyenylphosphatidylcholine (3 g/1000 kcal) or safflower oil, with or without 5 g/1000 kcal carbonyl iron. Parameters of oxidative stress (F2-isoprostanes, 4-hydroxynonenal, reduced glutathione), ubiquinol-10, ubiquinol-9 and vitamin E, as well as phosphatidylcholine species, were assessed by GC/MS and/or HPLC. Alcohol feeding increased pancreatic 4-hydroxynonenal three-fold, F2-isoprostanes and ubiquinol-9 by more than 70%, whereas it decreased total phospholipids, several phosphatidylcholine species, ubiquinol-10 and glutathione, especially in iron fed rats. Polyenylphosphatidylcholine prevented the rise in 4-hydroxynonenal and F2-isoprostanes, the decrease in dilinoleoylphosphatidylcholine and oleoyllinoleoylphosphatidylcholine and opposed the alcohol-induced decrease of glutathione; alpha-tocopherol remained unchanged. Iron had no significant effect except for decreasing ubiquinol-10 in the pancreas and increasing aminotransferases in the plasma. Thus, the alcohol-induced oxidative stress in the pancreas was shown to be prevented by polyenylphosphatidylcholine which may act, in part, by correcting the depletion of several phosphatidylcholine species.
Article Published Date : Mar 01, 1999
Study Type : Animal Study
Additional Links
Substances : Phosphatidylcholine : CK(101) : AC(22)
Diseases : Alcohol Toxicity : CK(337) : AC(125), Oxidative Stress : CK(3871) : AC(1382), Pancreatic Diseases : CK(21) : AC(8)
Pharmacological Actions : Antioxidants : CK(8430) : AC(3132)

Phosphatidylcholine (PC) plays an integral role in the structure and biology of cell membranes.
Choline metabolism. Choline and its metabolites serve three roles purposes: structural integrity and signaling roles for cell membranes, cholinergic neurotransmission (acetylcholine synthesis), and a source for methyl groups via its metabolite, trimethylglycine (betaine), which participates in the biosynthesis of S-adenosylmethionine (SAM)

Choline- Phosphatidylcholine
PubMed comprises more than 28 million citations for biomedical literature from MEDLINE, life science journals, and online books. 
In PubMed
There are 984  on Choline.
There are 55938 on 

21 Diseases Researched for Phosphatidylcholine/

Hepatitis C330
Cortisol: High110
Liver Fibrosis24
Alcohol Toxicity12
Alcoholic Liver Disease12
Aspirin-Induced Toxicity12
Chemically-Induced Liver Damage12
Cirrhosis: Liver12
Infant Infections12
Klebsiella Infections12
Neonatal Diseases and Abnormalities12
Oxidative Stress12
Pancreatic Diseases12
Breast Cancer11
HIV Infections11

9 Pharmacological Actions Researched forPhosphatidylcholine/ choline 
Anti-Inflammatory Agents110
Dermatologic Agents110
Antineoplastic Agents23
Interleukin-6 Downregulation12
Anti-HIV Agents11
Lipoxygenase Inhibitors11

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