Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Choline Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed2006

Parenteral nutrition-associated liver disease in adult and pediatric patients.

There are essentially 3 types of hepatobiliary disorders associated with parenteral nutrition (PN) therapy: steatosis, cholestasis, and gallbladder sludge/stones. Reported prevalence rates of PN-associated liver disease (PNALD) vary greatly, and there are distinct differences between adult and pediatric patients. Various etiologic factors have been evaluated for significance in contributing to PNALD, including enteral feeding history, septic events, bacterial overgrowth, length of intestinal resection, and prematurity/low birth weight. Etiologic factors specifically related to the PN formulation or nutrient intake have also been evaluated, including excessive calorie intake, dextrose-to-lipid ratio, amino acid dose, taurine deficiency, IV fat emulsion (IVFE) dose, carnitine deficiency, choline deficiency, and continuous vs cyclic infusion. Minor increases in serum aminotransferase concentrations are relatively common in patients receiving PN therapy and generally require no intervention. The primary indicator of cholestasis is a serum conjugated bilirubin >2 mg/dL. When a patient receiving PN develops liver complications, it is necessary to rule out all treatable causes and minimize other risk factors. All potential hepatotoxic medications and herbal supplements should be eliminated. Modifications to the PN regimen that may be helpful include reduction of calories, reduction of IVFE dose to <1 g/kg/d, supplementation of taurine in the infant, and use of cyclic infusion. Initiation of even small amounts of enteral nutrition and use of ursodiol may be beneficial in stimulating bile flow. In the long-term PN patient with severe and progressive liver disease, intestinal or liver transplantation may be the only remaining treatment option.

Adult↗
PubMed1987

Lipid peroxidation in choline-methionine deficiency.

A deficiency of choline and methionine is hepatocarcinogenic and is associated with an apparent increase in lipid peroxidation. In this study the susceptibility of microsomes and nuclei to ferritin-dependent lipid peroxidation is examined together with the status of the peroxidation-protective systems. Choline-methionine deficiency caused an increase in Se-independent GSH peroxidases (GSH transferase subunit 2) and membrane vitamin E but a decrease in Se-dependent GSH peroxidase and microsomal GSH peroxidase activity. Choline-methionine deficient microsomes and nuclei were 4-fold more susceptible to lipid peroxidation induced in vitro by physiological concentrations of ferritin/ascorbate/ADP; and the peroxidation was less effectively inhibited by GSH and soluble GSH peroxidases than controls. The results indicate that a decreased level of Se-dependent and membrane GSH peroxidases is involved in the increase in lipid peroxidation observed in choline-methionine deficiency.

Choline Deficiency↗
PubMed2004

Reactive oxygen species in choline deficiency-induced apoptosis in rat hepatocytes.

Choline deficiency (CD) is involved in hepatocellular carcinoma and CD-induced apoptosis may be implicated in cellular malignant transformation. In this report, we studied the effects of choline deficiency on generation of reactive oxygen species (ROS) using the fluorescent probe dichlorodihydrofluorescein diacetate and the possible role of ROS on CD-induced apoptosis in cultured CWSV-1 cells, an immortalized rat hepatocyte. This cell line is reported to become tumorigenic by step-wise culturing in lower levels of choline. Our data demonstrate that CD induces a time- and dose-dependent increase in ROS in CWSV-1 cells. The increase in ROS production may be related to dysfunction of the mitochondrial respiratory chain. Our data also demonstrated that ROS generation occurred before CD-induced apoptosis, suggesting ROS may play a key role in signaling CD-induced apoptosis in CWSV-1 cells.

Animals↗
PubMed1984

The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens.

Fischer 344 male rats fed a choline-methionine deficient diet for from 13 to 24 months developed a 100% incidence of putative preneoplastic hepatocyte nodules and a 51% incidence of hepatocellular carcinoma. The addition of 0.8% choline chloride completely prevented the development of both the nodules and the cancer. The diet contained no added known carcinogen. Analysis of the deficient and supplemented diets revealed no detectable volatile nitrosamines or nitrosamides, nitrite, nitrate or malonaldehyde, less than 0.9 p.p.b. aflatoxin B1 and barely detectable levels of Ames positive material with one strain of Salmonella typhimurium. These findings indicate that a dietary deficiency of choline and methionine can be a major rate limiting factor in the development of liver cancer.

Animals↗
PubMed1991

Evidence that remodeling of the fatty acids of phosphatidylcholine is regulated in isolated rat hepatocytes and involves both the sn-1 and sn-2 positions.

The remodeling of the fatty acyl moieties of phosphatidylcholine (PC) has been studied in choline-deficient and choline-supplemented hepatocytes prepared from a choline-deficient rat. Choline-deficient hepatocytes were prelabeled with [Me-3H]choline for 30 min and subsequently incubated for up to 12 h in the presence or absence of choline. Analysis of the molecular species of PC from choline-deficient cells showed that, at the end of the pulse, approx. 75% of the label was incorporated into palmitate-containing species and only approx. 16% of the labeled species contained stearate. During the chase period there was a redistribution of label and after 12 h approx. 56% of the total radioactivity was associated with palmitate containing species and 37% was recovered in stearate-containing species. A similar distribution of radioactivity was observed in choline-supplemented cells. Measurement of the specific radioactivity of the major molecular species of PC was consistent with a precursor-product relationship between palmitate-containing species and stearate-containing species with arachidonate or linoleate on the sn-2 position. A model is presented which takes into account remodeling of both the sn-1 and sn-2 positions of PC.

Animals↗
PubMed1991

Dietary choline manipulations and behavioural modifications in rats in the early stages of aging.

1. Behavioural effects of chronic manipulations of dietary choline in rats in the early stages of aging are reported. Rats were maintained on choline-deficient, low-choline and high-choline enriched diets. Two schedules of operant conditioning, representing "learning'h situations, plus an open field session were studied. 2. In the "temporal discrimination" test, the low-choline enriched group performed significantly better than controls while the deficient-choline group worse. The high-choline enriched group performed better than controls only in the second part of the test (where there was a stabilisation in behaviour). 3. In the "extinction" trials the high-choline enriched group retarded, while deficient-choline accelerated the extinction. In the open field sessions only the deficient-choline group, for the number of squares crossed, significantly differed from controls. 4. These observations lead us to suggest a general depressive effect in the rats on a choline-deficient diet, whereas with dietary choline supplements the effects on "learning" situations can be variable depending, on a large measure, on the test chosen.

Aging↗
PubMed1999

Endogenous liver carcinogenesis in the rat.

Carcinogenesis may be effected not only through exposure to exogenous stimuli but also by genetic and epigenetic influences derived from endogenous factors. In the latter case, the mechanisms are still largely obscure because of the limited availability of appropriate in vivo experimental models. However, continuous feeding of a diet deficient in choline and methionine is well known to cause hepatocellular carcinomas (HCC) in rats in the absence of any known exogenous carcinogens and can serve as a good research model. A semi-synthetic, choline-deficient, L-amino acid-defined (CDAA) diet, containing practically no choline and low methionine, induces HCC with a background of fatty liver and hepatocyte death, subsequent regeneration and fibrosis resulting in cirrhosis. Using the CDAA diet, we have revealed the participation of oxidative injury to DNA and other subcellular components and of alteration in intrahepatic signal transduction pathways in the mechanisms underlying this rat liver carcinogenesis model. In the present paper, the current understanding of endogenous rat liver carcinogenesis, due to dietary choline deficiency, is reviewed.

Amino Acids↗
PubMed1978

Assay for free and total choline activity in biological fluids and tissues of rats and man with Torulopsis pintolopessi.

The sensitive, specific growth response to choline activity of the thermophilic enteric yeast Torulopsis pintolopessi enables estimation of free and bound choline activity in rat and human fluids and tissues- as little as 10 ng/ml of choline is measurable. Unlike other microbial assays, estimation of unbound (free) choline activity is not influenced by methionine or phospholipids. The method also distinguishes differences in choline activity of fluids and tissues from choline-deficient and choline-replete rats. Free and bound choline activity in blood, red blood cells, plasma, and liver from choline-deficient rats were almost 2-fold lower than from choline-supplemented animals. Free and bound choline activity in whole brain from choline-deficient rats were signifigantly higher (more than 2-fold). The application of the T. pintolopessi method in studying choline status in man and reasons for high choline activity in brain of choline-deficient rats are suggested.

Adult↗
PubMed1984

Rapid lipid peroxidation in the nuclear fraction of rat liver induced by a diet deficient in choline and methionine.

A diet deficient in choline and methionine, known to produce hepatocellular carcinoma in the absence of any added chemical carcinogen, induced lipid peroxidation in the nuclear fraction of the liver when fed to male Fischer 344 rats. This lipid peroxidation was detected within 1 day of feeding the diet by the appearance of diene conjugates and increased progressively up to 3 days. It was prevented completely by the addition of choline chloride to the diet. The close proximity of DNA may make it a possible target for attack by free radicals.

Animals↗
PubMed2001

Regeneration of liver with marked fatty change following partial hepatectomy in rats.

Resection of liver for primary and metastatic tumors and living donor liver transplantation has become a common clinical practice. The success of recovery depends on the regeneration and functions of the remnant liver. However, information on the regenerative potential of liver with steatosis and steatohepatitis, a common clinical problem in this country, is incomplete. Therefore, we evaluated regeneration after two-thirds partial hepatectomy (PH) in male F-344 rats with marked steatosis and mild steatohepatitis induced by feeding choline-deficient diet. Choline-deficient rats and control rats were killed at 24, 36, 48, 72, and 96 h after PH. Liver regeneration was determined by measuring mitotic activity and bromodeoxyuridine (BrdU) labeling in hepatocytes. Livers of rats maintained on the choline-deficient diet showed marked steatosis and mild steatohepatitis. In these animals the levels of serum and liver triacylglycerols (TG) were low and very high, respectively, when compared to controls. In control rats mitotic and BrdU labeling indices were maximal at 24 h followed by a rapid decline, whereas in choline-deficient rats both these indices increased significantly at 36 h and decreased gradually over the next 60 h. By 96 h the size of livers in both groups was comparable. The results of this study indicate that regeneration in the liver of rats with marked steatosis is not impaired.

Animals↗
PubMed1991

Evidence that the rate of phosphatidylcholine catabolism is regulated in cultured rat hepatocytes.

The regulation of phosphatidylcholine (PC) catabolism has been studied in choline-deficient rat hepatocytes. Supplementation of choline-deficient hepatocytes, prelabeled with [3H]choline, with 100 microM choline increased the rate of PC catabolism by approx. 2-fold. The major product of PC degradation was glycerophosphocholine in both choline-deficient and choline-supplemented cells. Choline supplementation decreased the radioactivity recovered in lysoPC by 50%. This effect was accompanied by a 2-fold increase of labeled glycerophosphocholine. Comparable results were obtained when PC of the cells was prelabeled with [3H]methionine or [3H]glycerol. The activity of phospholipase A in cytosol, mitochondria and microsomes isolated from choline-deficient rat liver was similar to the activity in control liver, when determined with [3H]PC vesicles as the substrate. Measurement of the activity of phospholipase A with endogenously [3H]choline-labeled PC showed that the formation of lysoPC in mitochondria isolated form choline-supplemented cells was 40% lower than in choline-deficient cells. Alternatively, the formation of [3H]glycerophosphocholine and [3H]choline in microsomes from choline-supplemented cells was significantly higher (1.4-fold) than in microsomes from choline-deficient cells. These results suggest that the rate of PC catabolism is regulated in rat hepatocytes and that the concentration of PC might be an important regulatory factor.

Animals↗
PubMed1992

Dietary choline supplementation increases the density of nicotine binding sites in rat brain.

The objective of these studies was to determine whether the chronic administration of choline, like the chronic administration of nicotine, increased the density of nicotine binding sites in brain. To accomplish this, rats were maintained on a choline-deficient (0% choline chloride), basal choline (0.2% choline chloride) or choline-supplemented (2.0% choline chloride) diet for 30 days or were fed a standard rodent chow and received injections of saline or nicotine (3.6 mumol/kg s.c.) twice daily for 10 days. Membranes from striatum, hippocampus and frontal cortex were isolated, and the binding of L-(-)-[N-methyl-3H]nicotine (0.5-60 nM) was studied. A single binding site for nicotine was evident for all brain regions from all animals studied with a dissociation constant (Kd) of approximately 2 to 5 nM. Chronic supplementation with choline, which increased circulating choline levels by 92%, did not alter binding affinity, but increased significantly the maximal number (Bmax) of nicotine binding sites in cortical and hippocampal membranes by 20 and 73%, respectively, compared to animals fed the basal choline diet; the Bmax in striatal membranes was unaltered. Nicotine binding parameters for membranes from animals maintained on the choline-deficient diet were not different from those maintained on the basal diet. The chronic administration of nicotine did not alter binding affinity, but increased significantly the maximal density of nicotine binding sites in striatal and cortical preparations by 47 and 18%, respectively; the Bmax in hippocampal membranes was unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Effects of chronic manipulations of dietary choline on dynamic behavioural situations.

1. The modifications in rat behaviour caused by chronic manipulations of dietary choline were studied in two schedules of operant conditioning. Adult rats were maintained on choline-deficient, low-choline and high-choline enriched diets. 2. In the "periodic conditioning" test, the schedule of reinforcement was changed from a fixed ratio to a fixed interval schedule. In the "reversal" test the contingency for food delivery was switched four times from one lever to the other in a two lever Skinner box. 3. In the "periodic conditioning" test, control and treated groups showed the same reduction of responses/reinforcement from the beginning to the end of trial. The time-course reduction of responses/reinforcement became significant in the high-choline (331 mg/kg/day) and deficient-choline groups earlier than in the low-choline (75 mg/kg/day) enriched and control groups. 4. In the "reversal" test, the low-choline (110 mg/kg/day) enriched diet improved the reinforced responses in the IV reversal; the high-choline (330 mg/kg/day) diet gave a significant impairment of the reinforced responses in the III and IV reversals. The deficient-choline diet caused a reduced number of the total responses and a worsening of the reinforced responses in the II, III and IV reversals.

Animals↗