scholarly journals Dietary choline deficiency alters global and gene‐specific DNA methylation in the developing hippocampus of mouse fetal brains

2006 ◽  
Vol 20 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Mihai D. Niculescu ◽  
Corneliu N. Craciunescu ◽  
Steven H. Zeisel
Keyword(s):  
Dna Methylation ◽  
Choline Deficiency ◽  
Dietary Choline

scholarly journals Maternal dietary choline deficiency alters angiogenesis in fetal mouse hippocampus

2010 ◽  
Vol 107 (29) ◽  
pp. 12834-12839 ◽  
Author(s):  
M. G. Mehedint ◽  
C. N. Craciunescu ◽  
S. H. Zeisel
Keyword(s):  
Choline Deficiency ◽  
Fetal Mouse ◽  
Mouse Hippocampus ◽  
Dietary Choline

INFLUENCE OF DIETARY CHOLINE AND PROTEIN ON THE LEVEL OF PHOSPHOLIPID IN THE SERUM OF THE RAT

1957 ◽  
Vol 35 (1) ◽  
pp. 845-852 ◽  
Author(s):  
Bruno Rosenfeld ◽  
Jessie M. Lang
Keyword(s):  
Protein Content ◽  
Significant Rise ◽  
Albino Rats ◽  
Choline Deficiency ◽  
Serum Phospholipid ◽  
Liver Lipids ◽  
Total Liver ◽  
Dietary Choline

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.

Dietary Choline Deficiency as a New Model to Study the Possible Role of Free Radicals in Acute Cell Injury and in Carcinogenesis

1987 ◽  
pp. 303-308 ◽  
Author(s):  
Amiya K. Ghoshal ◽  
T. H. Rushmore ◽  
D. Ghazarian ◽  
Amit Ghoshal ◽  
V. Subrahmanyan ◽  
...  
Keyword(s):  
Free Radicals ◽  
Cell Injury ◽  
Choline Deficiency ◽  
New Model ◽  
Dietary Choline

scholarly journals Supplementation of Choline-Deficient Diet With Pterostilbene Attenuates Cancer Development and Epigenetic Dysregulation of Gene Expression in Rat Livers

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 280-280
Author(s):  
Barbara Stefanska ◽  
Cayla Boycott ◽  
Megan Beetch ◽  
Aline de Conti ◽  
Igor Pogribny
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Liver Cancer ◽  
Regulation Of Gene Expression ◽  
Cancer Development ◽  
Control Group ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Development Fund ◽  
Increased Risk

Abstract Objectives Nearly 40% of humans have polymorphisms in genes involved in choline metabolism which makes them prone to developing choline deficiency and increased risk for liver damage and liver cancer. Choline is a source of methyl groups needed for many steps in metabolism and epigenetic regulation of gene expression. Although epigenetic aberrations are known to be induced by choline deficiency, it remains unknown how to reverse the changes and attenuate symptoms. Interestingly, certain dietary compounds such as polyphenols have been demonstrated to reverse aberrant epigenetic patterns and exert anti-cancer action. In the present study, we investigate the effects of pterostilbene (PTS) on liver cancer development in rats fed choline-deficient diet and explore mechanisms underlying these effects. Methods Fischer 344 rats were fed a choline-sufficient (CSAA, healthy control group), a choline-deficient (CDAA, cancer group) L-amino acid-defined diet or a CDAA diet supplemented with PTS (134 mg/kg BW/day) (n = 6 per group). At the end of 52 weeks, analyses of liver nodules and histopathological features were performed followed by genome-wide investigation of gene expression in livers using RNA sequencing. DNA methylation was assessed by pyrosequencing. Results A total of 708 genes were significantly differentially expressed in CDAA + PTS group as compared with CDAA group. Among 351 upregulated genes were Bhmt (4.5-fold), G6pc (3.1-fold), and Aldh1l1 (2.6-fold). These metabolism-related genes were significantly downregulated in CDAA vs. CSAA group and their suppression was associated with liver cancer in previous reports. Among 357 genes found to be significantly downregulated by PTS were strong oncogenes such as Mmp12 (2-fold), Myc (1.9-fold) and Mmp27 (1.8-fold). We found PTS-mediated downregulation of Mmp12, that was a top gene upregulated in CDAA vs. CSAA, coincided with 43% hypermethylation of Mmp12 promoter. Conclusions Our findings demonstrate that PTS-mediated changes in gene expression could correspond to changes in DNA methylation of gene regulatory regions and could at least partially explain the observed attenuation of cancer development due to choline deficiency. Funding Sources UBC VP Academic Award, CFI John. R. Evans Leaders Fund, and BC Knowledge Development Fund granted to BS.

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