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Results for “Choline Deficiency”

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PubMed1988

Effects of 5-azacytidine and methyl-group deficiency on NAD(P)H: quinone oxidoreductase and glutathione S-transferase in liver.

Treatment with 5-azacytidine or dietary methyl-group deficiency effected DNA hypomethylation in mouse liver. With these treatments, NAD(P)H: quinone oxidoreductase (EC 1.6.99.2) and some glutathione S-transferase (EC 2.5.1.18) activities were over-expressed, lactate dehydrogenase (EC 1.1.1.27) activity was unaffected and the level of cytochrome P-450 was decreased. The 5-azacytidine induction of NAD(P)H: quinone oxidoreductase was significantly suppressed by puromycin, suggesting that increased enzyme activity results from an elevated level of enzyme-protein synthesis. Regulation at the transcriptional level was revealed by a substantial increase in mRNA of NAD(P)H: quinone oxidoreductase, as shown by Northern-blot analysis. The enzyme pattern observed with 5-azacytidine and with the (carcinogenic) dietary methyl-group deficiency resembles that found in hepatic nodules.

Animals↗
PubMed1998

Biochemical and evolutionary significance of phospholipid methylation.

All nucleated mammalian cells synthesize phosphatidylcholine from choline via the CDP-choline pathway. Hepatocytes have a second pathway for the synthesis of phosphatidylcholine, a stepwise methylation of phosphatidylethanolamine, catalyzed by phosphatidylethanolamine N-methyltransferase and encoded by the Pempt gene. We report that when Pempt-deficient mice were fed a choline-deficient diet for 3 days, severe liver pathology occurred apparently due to a lack of phosphatidylcholine biosynthesis. The hepatic concentration of phosphatidylcholine decreased by 50% compared with wild type mice on the diet. The levels of plasma triacylglycerols and cholesterol were decreased by greater than 90% in the Pempt-deficient mice. We suggest that the Pempt gene has been maintained during evolution to provide phosphatidylcholine when dietary choline is insufficient, as might occur during starvation or pregnancy.

Animals↗
PubMed1980

Effects of linolenic acid deficiency on the fatty acid patterns in plasma and liver cholesteryl esters, triglycerides and phospholipids in female rats.

These experiments were performed to measure the effects of linolenate deficiency upon neutral lipids of plasma and liver, and to search for a metabolic interaction between dietary choline and linolenic acid. Rats were fed for two generations on a linolenic acid-deficient diet containing methyl linoleate as the only source of lipid. Control rats were supplemented with methyl linolenate. Second-generation linolenate-deficient rats and control rats were fed low-methionine, choline-deficient diets for 2 weeks. Half the animals in each group were given choline-supplemented diets. Plasma and liver total cholesterol, esterified cholesterol, triglyceride and major phospholipid classes, and the fatty acids of these classes were measured. Linolenic acid deficiency reduced the concentrations of plasma triglycerides in both choline-deficient and choline-supplemented rats. Evidence for a metabolic interaction between choline and linolenic acid was not obtained because the rats responded very weakly to the choline deficiency. Linolenate deficiency reduced the proportions of n-3 fatty acids, particularly 22:6n-3, in all the lipids analyzed.

Animals↗
PubMed2003

Vitamin B12 is a strong determinant of low methionine synthase activity and DNA hypomethylation in gastrectomized rats.

BACKGROUND/AIMS: The respective influence of folate and vitamin B12 deficiency on MTR activity and transcription, and on DNA methylation is not clearly established. The aim of this study was to assess the respective influence of folate and vitamin B12 deficiency on MTR transcription and activity, and on DNA methylation. METHODS: Sixty-one rats were administered normal diet or diet deficient in choline, methionine, folic acid and vitamin B12. Forty-seven of them underwent total gastrectomy or ileal resection. RESULTS: Low vitamin B12 was observed only in gastrectomized rats. Low folate was observed in rats under deficient diet. Total MTR activity (holo- + apoenzyme) was lowered only with vitamin B12 level <200 pmol/l (p=0.0002), while the ratios of total vs. holo-MTR activity and of transcripts MTR vs. GAPDH (RT-PCR) were unchanged. Vitamin B12 was the single determinant of low MTR (lower quartile, odds ratio=15.75, p=0.0017). Low MTR and low vitamin B12 were the two determinants of DNA hypomethylation (lower quartile) (odds ratio=17.07, p=0.0006, and odds ratio=7.31, p=0.006, respectively). CONCLUSION: Vitamin B12 affects MTR expression by a non-transcriptional mechanism different from a protective effect on MTR proteolysis. It is also a strong determinant of DNA hypomethylation.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1993

Acute hepatic response to aflatoxin B1 in rats fed a methyl-deficient, amino acid-defined diet.

In order to evaluate the relative contribution of aflatoxin B1 (AFB1)-induced toxicity towards a methyl-deficient diet influenced AFB1 carcinogenesis, a no-observed-effect-level (NOEL) for AFB1, with reference to liver damage, was determined in rats fed a nutritionally complete amino acid-defined basal (CMS) diet or a choline-methionine-deficient (CMD) diet. After 3 weeks of dietary treatment, male Fischer 344 rats received a single, oral dose of AFB1 in the range of 100-600 pg/kg body weight. At 24, 48 and 72 h after AFB1 treatment, six serum biochemical parameters were analysed in parallel with histological examination of liver sections. In rats fed the CMS diet and receiving 250-600 micrograms/kg AFB1, serum levels of glutamyl oxalo-transaminase (SGOT), glutamyl pyruvic transaminase (SGPT), alkaline phosphatase (ALP) and total bilirubin increased, glucose levels decreased and gamma glutamyl transpeptidase (GGT) levels remained unchanged over the 72-h period following mycotoxin treatment. However, at 100 micrograms/kg AFB1, these serum parameters remained at control levels. Pathological examination of liver sections indicated no significant lesions at 100 micrograms/kg AFB1 confirming this as the non-necrogenic dose or NOEL in CMS diet group rats. In contrast, in CMD diet fed rats, serum or pathology data showed no obvious time- or dose-response to mycotoxin treatment, extensive hepatic lipidosis in response to dietary treatment being the only predominant lesion in this diet group. The milder response of CMD rat livers to a single dose of AFB1 suggest a possible reduction in the susceptibility of these livers to AFB1 toxicity.

Aflatoxin B1↗
PubMed1993

Lipotrope-modified diets enhance nitrosomethylurea-induced mammary carcinogenesis in female rats.

This study was conducted to determine the effects of lipotrope-modified (deficient or supplemented) diets on nitrosomethylurea- (NMU) induced mammary tumorigenesis. Eighty female Sprague-Dawley rats (4 wks old) were assigned to one of the following groups: control-synthetic diet (CSD), containing all required lipotropes; choline-methionine-deficient diet (CMD); methyl-deficient diet (MDD), lacking all lipotropes; and methyl-supplemented diet (MSD), containing twice as much of each lipotrope as the CSD diet. All animals were injected with NMU after a three-week dietary treatment period. MDD and MSD groups had shorter tumor latency periods (73 and 74 days, respectively) than the CSD group (105 days). Number of tumors per rat was significantly increased in the MDD group (4.6) compared with CSD (1.6), CMD (2.1), and MSD (2.5) groups. The results indicate that dietary manipulation of lipotropes in young female rats enhanced NMU-induced mammary tumorigenesis.

Animals↗
PubMed1993

Low plasma free choline is prevalent in patients receiving long term parenteral nutrition and is associated with hepatic aminotransferase abnormalities.

Hepatic transaminase abnormalities have been previously reported in patients receiving long term total parenteral nutrition (PN). We sought to determine if such abnormalities are caused by choline deficiency-induced hepatocyte damage. In 41 subjects (19 male, 22 female) aged 45.1 +/- 24.3 years (range 0.1-79 years) who have received PN for 5.5 +/- 4.7 years (range 0.1-14.5 years). We determined plasma free and phospholipid bound choline levels, serum albumin, ALT and AST. We also determined the daily volume of intravenous lipid emulsion received by the patients as well as the concentration of free choline and phospholipid bound choline in the lipid emulsion. Plasma free choline was low in 33 41 subjects (mean 7.15 +/- 2.5 nmol/ml, range 3.3-15.6, normal 11.4 +/- 3.7). Phospholipid bound choline was normal in 34 41 subjects (mean 2157 +/- 620 nmol/ml, range 1026-3887, normal 2364 +/- 774). Elevations in ALT and AST were significantly correlated with plasma free choline (r = -0.34, p = 0.03, r = -0.37, p = 0.02 respectively) but not with phospholipid bound choline. No relationship was found between age, PN duration or daily volume of intravenous lipid and plasma free or phospholipid bound choline. The lipid emulsion contained 24 +/- 6 nmol/ml of free choline and 11 630 +/- 552 nmol/ml of phospholipid bound choline. We conclude that low plasma free choline is prevalent in patients receiving long term PN and this abnormality is associated with elevated serum aminotransferases. Furthermore, intravenous lipid emulsion is an inadequate source of choline for this patient group.

Journal Article↗
PubMedDate not supplied

[Influence of qualitatively different fats on the level of cholesterol and phospholipids in the blood serum and liver on rats in choline-protein insufficiency].

The effect of lard and sunflower oil making part of a cirrhogenic ration with a high content of fat and deficient protein and choline on the level of total and esterified cholesterol and phospholipids in the blood serum and liver was studied. The experiments lasted for 150 and 210-240 days. Changes in the level of cholesterol and phospholipids in the blood serum and liver of the rats were noted to occur from the first days of developing fat dystrophy (fatty degeneration) of the liver, these changes gaining in intensity with lengthening of the test periods and progressive development of the pathological process. The quality of the fat influenced the extent of the upset cholesterol and phospholipids metabolism, since the saturated fat which accelerated and intensified the development of lipohepatosis and cirrhosis caused a significantly greater accumulation of the cholesterol ethers in the liver and reduction of these ethers, as well as of phospholipids in the serum. An addition of choline to the rations prevented the development of lipohepatosis, but failed to avert upsets of the lipids metabolism.

Animals↗