Effect of phenobarbital on the development of fatty livers In choline-deficient rats

1970 ◽  
Vol 48 (11) ◽  
pp. 1284-1285 ◽  
Author(s):  
A. Chalvardjian
Keyword(s):  
Hepatic Cell ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Fatty Livers ◽  
Phenobarbital Administration ◽  
Phospholipid Pool

The increase in hepatic phospholipid pool induced by phenobarbital did not affect the hepatic accumulation of fat produced by feeding rats a choline-deficient diet for 4 days. This lack of effect suggests that phenobarbital administration does not increase the choline requirement of rats, and/or that phenobarbital and choline deficiency act on different loci within the hepatic cell independently of each other.

CHOLINE DEFICIENCY IN THE GUINEA PIG

1957 ◽  
Vol 35 (1) ◽  
pp. 1-6 ◽  
Author(s):  
R. J. Young ◽  
C. C. Lucas
Keyword(s):  
Guinea Pig ◽  
Body Fat ◽  
Guinea Pigs ◽  
Liver Fat ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Methyl Group ◽  
Complete Diet ◽  
Total Body Fat ◽  
Total Body

Young guinea pigs (4–6 days of age) fed a choline-deficient diet grew slowly and died within 3 to 4 weeks, at which time the livers showed only traces of stainable fat. Animals fed the diet supplemented with choline grew at the rate of 5.5 to 6.0 g. per day. Guinea pigs transferred from a complete diet to a choline-deficient diet after 3 to 4 weeks suffered an immediate retardation in growth but no mortality occurred (up to 6 weeks). A decrease in total body fat was noted. After 4 weeks, stainable fat was present in the liver. A small but definite increase in total liver fat occurred at 6 weeks. The guinea pig, like the chick, is unable to place the first methyl group on the ethanolamine moiety of choline, but betaine plus monomethylaminoethanol was as effective as choline in overcoming a deficiency of the latter.

Metabolism of Choline by Slices of Fatty Livers From Choline-Deficient Rats

1958 ◽  
Vol 193 (2) ◽  
pp. 431-434
Author(s):  
E. Douglas Rees ◽  
Daniel L. Kline
Keyword(s):  
Oxygen Uptake ◽  
Fatty Liver ◽  
Deficient Diet ◽  
Betaine Aldehyde ◽  
Liver Slices ◽  
Fatty Livers

Fatty livers were produced in rats by a choline-deficient diet and the metabolism of slices from the livers was studied. The addition of choline increased the qo2 of slices of fatty liver more than it did the qo2 of control slices. The qco2 and R.Q. of both types of slices decreased in the presence of choline. For both the control and the fatty liver slices, an increased concentration of an unidentified material, (probably not betaine aldehyde), which reacted with 2,4-dinitrophenylhydrazine was found whenever the respiration medium contained choline. Fatty liver slices produced more of this substance relative to oxygen uptake.

scholarly journals Choline Deficiency Attenuates Body Weight Gain and Improves Glucose Tolerance in ob/ob Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Gengshu Wu ◽  
Liyan Zhang ◽  
Tete Li ◽  
Gary Lopaschuk ◽  
Dennis E. Vance ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Fat Mass ◽  
Body Weight Gain ◽  
Genetic Defect ◽  
Plasma Glucagon ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Insulin Tolerance

Previous studies demonstrated that choline supply is directly linked to high-fat-diet-induced obesity and insulin resistance in mice. The aim of this study was to evaluate if choline supply could also modulate obesity and insulin resistance caused by a genetic defect. Eight-week-old male ob/ob mice were fed for two months with either choline-deficient or choline-supplemented diet. Tissue weight including fat mass and lean mass was assessed. Intracellular signaling, plasma glucagon and insulin, and glucose and insulin tolerance tests were also investigated. The choline-deficient diet slowed body weight gain and decreased fat mass. Choline deficiency also decreased plasma glucose level and improved glucose and insulin tolerance although fatty liver was exacerbated. Increased adipose lipolytic activity, decreased plasma glucagon and reduced expression of hepatic glucagon receptor were also observed with the choline-deficient diet. Our results demonstrate that a choline-deficient diet can decrease fat mass and improve glucose tolerance in obese and diabetic mice caused by a genetic defect.

scholarly journals Starvation Impairs Antioxidant Defense in Fatty Livers of Rats Fed A Choline-Deficient Diet

2000 ◽  
Vol 130 (9) ◽  
pp. 2131-2136 ◽  
Author(s):  
Ignazio Grattagliano ◽  
Gianluigi Vendemiale ◽  
Paolo Caraceni ◽  
Marco Domenicali ◽  
Bruno Nardo ◽  
...  
Keyword(s):  
Antioxidant Defense ◽  
Deficient Diet ◽  
Fatty Livers

Histological Differentiation of Fatty Livers Produced by Threonine or Choline Deficiency

1954 ◽  
Vol 53 (4) ◽  
pp. 469-480 ◽  
Author(s):  
Hipólito Niño-Herrera ◽  
Alfred E. Harper ◽  
Conrad A. Elvehjem
Keyword(s):  
Choline Deficiency ◽  
Histological Differentiation ◽  
Fatty Livers

Impairment of plasma glycoprotein synthesis in choline deficiency compared with effects of carbon tetrachloride intoxication

1968 ◽  
Vol 46 (3) ◽  
pp. 499-505 ◽  
Author(s):  
Sailen Mookerjea
Keyword(s):  
Carbon Tetrachloride ◽  
Plasma Proteins ◽  
Specific Radioactivity ◽  
Starch Gel Electrophoresis ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Glycoprotein Synthesis ◽  
Carbon Tetrachloride Intoxication ◽  
Starch Gel ◽  
Plasma Glycoprotein

The incorporation of glucosamine-1-14C into plasma proteins is impaired in rats within 2 days when they are fed a choline-deficient diet. Separation of plasma proteins by starch-gel electrophoresis, and autoradiography of the dried gels, showed four labelled areas (glycoproteins). In choline deficiency there was visual evidence of depletion of radioactivity in the fast α-globulin area, a finding confirmed by the specific radioactivity of proteins eluted from electrophoretic zones of the starch gel. Within 4 h after ingestion of carbon tetrachloride, the synthesis of plasma glycoprotein was reduced by 90% and labelling of all four glycoprotein areas on dried starch gel autoradiograms virtually ceased. The results suggest that the defect in glycoprotein synthesis in carbon tetrachloride intoxication is nonspecific, whereas in choline deficiency the impairment is specific and localized in the fast α-globulin fraction. The results suggest a limiting role of a glycoprotein in the pathway of plasma lipoprotein synthesis.

Reduction in VLDL, but not HDL, in plasma of rats deficient in choline

1990 ◽  
Vol 68 (2) ◽  
pp. 552-558 ◽  
Author(s):  
Zemin Yao ◽  
Dennis E. Vance
Keyword(s):  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
High Density ◽  
Plasma Lipoproteins ◽  
Male Rats ◽  
High Density Lipoproteins ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Apo B

We have analyzed plasma lipoprotein levels in young male rats fed a choline-deficient diet for 3 days. We confirmed previous studies that choline deficiency promotes 6.5-fold accumulation of triacylgycerol in the liver (23.9 ± 6.0 versus 3.69 ± 0.92 μmol/g liver) and reduction of triacylglycerol concentration in plasma by 60% (0.17 ± 0.04 versus 0.46 ± 0.10μmol/mL plasma). Agarose gel electrophoresis showed that the plasma very low density lipoprotein (VLDL) levels were reduced in choline-deficient rats, but the concentration of plasma high density lipoproteins (HDL) was not affected. Sodium dodecyl sulfate – polyacrylamide gel electrophoresis of fractionated plasma lipoproteins revealed that the concentrations of apolipoproteins (apo) BH, BL, and E in VLDL from choline-deficient rats were 37.1, 11.0, and 37.2% of normal levels, respectively. In contrast, the amount of apo A-I, the major one in HDL, was almost unchanged. Correspondingly, there were decreased lipid (mainly phosphatidylcholine and triacylglycerol) levels in VLDL from choline-deficient rats, but no change in the levels of phosphatidylcholine, cholesterol, and cholesterol ester in HDL. There were similar levels of apo B and E (components of VLDL) in homogenates of livers from normal and choline-deficient rats, as determined by immunoblotting. These results support the hypothesis that choline deficiency causes reduction of VLDL, but not HDL, levels in plasma as a consequence of impaired hepatic VLDL secretion.Key words: choline deficiency, very low and high density lipoproteins, apolipoproteins, rat plasma.

STUDIES ON THE RAPID ACCUMULATION OF TRIGLYCERIDE IN THE LIVER IN CHOLINE DEFICIENCY

1965 ◽  
Vol 43 (10) ◽  
pp. 1733-1744 ◽  
Author(s):  
Sailen Mookerjea
Keyword(s):  
Acute Phase ◽  
Early Phase ◽  
Liver Perfusion ◽  
State Level ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Rapid Accumulation ◽  
Triphasic Pattern ◽  
Isolated Liver ◽  
Intact Rats

Studies with isolated liver perfusion preparations showed that, during 5 to 21 days of choline deficiency (acute phase), the livers fail to release any triglyceride into the perfusate, whereas during 1 to 2 days (early phase) and during 28 to 60 days of choline deficiency (prolonged phase), they tend to release triglyceride into the perfusate at a nearly normal rate. The rate of deposition of hepatic triglyceride in intact rats fed a choline-deficient diet showed a progression complementary to this triphasic pattern of triglyceride release, i.e. an early phase of slow triglyceride deposition and an acute phase of rapid accumulation followed by the establishment of a higher steady-state level. In the perfusion experiments changes in phospholipid levels in the perfusate followed the same pattern as the triglyceride levels. Increased uptake of free fatty acids by the choline-deficient livers was most marked after 2 days.In vitro additions of choline and several choline derivatives to the 5-day choline-deficient liver perfusion system were unable to restore triglyceride release. Similar studies with blood obtained from choline-supplemented rats showed a very significant restoration of triglyceride release into the perfusate.

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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