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Results for “Choline Deficiency”

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PubMed1991

Nutritional model of hepatocarcinogenesis. Rats fed choline-devoid diet.

Rats fed a choline-devoid diet as the sole treatment develop hepatocellular carcinomas, the pathogenesis of which appears to reside exclusively in effects of the diet on the liver. Among the latter, most prominent is the induction of repeating cycles of liver cell injury, death, and regeneration. Two other models have been described recently in the literature, in which development of hepatic neoplastic lesions occurs after protracted periods of liver cell injury, death, and regeneration, without exposure of the animals to chemical carcinogens. The possibility is considered that an abnormal increase in cell turnover may result in all of the genomic alterations that are required for initiation, promotion, and neoplastic transformation of liver cells in these models of hepatocarcinogenesis. The possible involvement, in the same models, of endogenously initiated liver cells also is discussed briefly.

Animals↗
PubMed1995

In vivo proton magnetic resonance spectroscopy in a case of Reye's syndrome.

A case of a 14-year-old boy with Reye's syndrome (RS) and complete neurologic recovery is presented. 1H magnetic resonance spectroscopy was performed on days 1 (admission to ICU), 8 and 62: During the acute phase of RS substantial cerebral metabolic imbalances were observed and their normalization monitored. The spectra from day 1 featured extremely high glutamine content (approximately 18 mmol/kg excess) and low concentrations of choline compounds pounds (approximately 1 mmol/kg deficit). Also some excess lactate was present. The subsequent spectra demonstrated the return to an almost normal brain metabolite profile.

Adolescent↗
PubMed1979

A simplified procedure for the determination of betaine in liver.

A convenient procedure for the determination of hepatic betaine levels is described. The method takes advantage of ethanol precipitation to rid acidified tissue extracts of interfering substances. Betaine is reacted with potassium triiodide to form betaine periodide, which is selectively precipitated via pH adjustment. The precipitate of betaine periodide is dissolved in ethylene dichloride and measured spectrophotometrically. The method is specific, accurate, and simple and showed recoveries of from 97 to 103% at two different levels of added betaine. The applicability of the method was shown when it was demonstrated that diets containing different amounts of choline influenced levels of hepatic betaine.

Animals↗
PubMed1992

Changes in fatty acid composition of phospholipids from liver microsomes and nuclei in rats fed a choline-free diet.

Male F-344 rats were fed a choline-free (CF) diet, and changes in phospholipid content, phospholipid fatty acids and phospholipase A2 activity in liver nuclei and microsomes were examined during the first 72 hr. Both nuclei and microsomes showed a decrease in phosphatidylcholine (PC) content. Microsomes showed an increase in PC arachidonate while nuclei showed a decrease. Also, microsomes showed increased activity of phospholipase A2 (PLA2) while nuclei did not. These observations are consistent with the hypothesis that the absence of diene conjugates in liver microsomes in the rats on the CF diet may reflect the increased rate of removal of peroxidized fatty acids by phospholipase A2.

Animals↗
PubMed1999

The Lewy body variant of Alzheimer's disease: clinical, pathophysiological and conceptual issues.

In 1923, Friedrich H. Lewy described dementia with Lewy bodies in a large proportion of his patients with paralysis agitans which had co-incident plaques and neurofibrillary tangles. The potential contribution of Lewy bodies to a dementia syndrome with fluctuating course, visual hallucinations, Parkinsonian features and neuroleptic hypersensitivity was rediscovered many decades later. The comorbidity of Alzheimer's and Parkinson's disease is not uncommon as both diseases show an exponential increase with advancing age and their coincidence is of great clinical importance. The combination of a cholinergic deficit--which is particularly severe due to the double pathology targeting the basal nucleus of Meynert--and a dopaminergic deficit requires cholinergic and cautious dopaminergic treatment. Excessive dopamine (L-dopa), antidopaminergic (neuroleptic) or anticholinergic treatment (anti-Parkinson or neuroleptic medication) may further complicate the condition, worsen extrapyramidal, psychotic or cognitive disturbances and even lead to a neuroleptic malignant syndrome.

Aged↗
PubMed2005

Dopamine D2 receptor plays a role in memory function: implications of dopamine-acetylcholine interaction in the ventral hippocampus.

RATIONALE: The role of the hippocampal dopaminergic system in mnemonic function has not been clarified yet. OBJECTIVE: We previously reported that the dopamine D2 receptor (D2R) is involved in the regulation of acethylcholin (ACh) release in the hippocampus. In this study, we further investigated ACh-dopamine (DA) interaction in the hippocampus and its involvement in mnemonic function. METHODS: For experiment 1, rats fed with Cholin (Ch)-deficient chow were used. We examined the effects of D2R antagonist, raclopride, on cognitive performance using a passive avoidance task. We further carried out in vivo microdialysis to assess the effect of infusion of D2R agonist, quinpirole, into the ventral hippocampus on its capacity to release ACh. For experiment 2, rats fed with normal chow were used. The performance of a radial arm maze task was assessed to examine the effects of hippocampal injection of D2R agonist, quinpirole, on memory impairment induced by scopolamine, a muscarinic ACh antagonist. RESULTS: In experiment 1, rats fed with Ch-deficient chow showed impaired performances indicated by prolonged latency on retention trials of a passive avoidance task following the hippocampal injection of D2R antagonist, and showed reduced capacity to release ACh following the injection of D2R agonist compared with rats fed with normal chow. In experiment 2, memory impairment induced by the intraperitoneal injection of scopolamine was ameliorated by the injection of D2R agonist into the ventral hippocampus. CONCLUSION: These results indicate the possible involvement of hippocampal ACh-DA interaction in mnemonic processing.

Acetylcholine↗
PubMed1999

Nutrition and liver diseases.

Malnutrition and micronutrient deficiencies are common in patients with liver diseases. The pathogenesis of protein-energy malnutrition in cirrhosis involves many factors, including poor oral intake, malabsorption, and metabolic abnormalities similar to stress. Encephalopathy may complicate cirrhosis but is usually not caused by diet. Protein restriction is only necessary in rare patients with refractory encephalopathy. The use of branched-chain amino-acid solutions is not supported by the literature. Chronic liver diseases without cirrhosis are not usually associated with protein-energy malnutrition, but vitamin and mineral deficiencies are common, especially with significant cholestasis. Fatty liver may result from excessive triglyceride uptake and production by the liver or by a secretory defect. Therapy for fatty liver depends on its cause. Chronic total parenteral nutrition may induce fatty liver and inflammation especially in patients with short-bowel syndrome. Deficiency of choline in parenteral nutrition has been proposed as the mechanism for liver disease. Acute liver diseases such as fulminant hepatic failure or alcoholic hepatitis are considered hypercatabolic diseases and thus require prompt nutritional intervention with a high-calorie enteral or parenteral formula. In fulminant hepatic failure, low-protein, fluid-restricted formulas are recommended.

Chronic Disease↗
PubMed1980

13C-NMR detection of lipid polymorphism in model and biological membranes.

1. The application of the 13C-NMR technique to the study of lipid polymorphism is described for various model and biological membranes. 2. The 13-C-NMR line-width of various resonances of the lipid molecule and sensitive to the bilayer in equilibrium hexagonal and the bilayer in equilibrium 'isotropic' phase transition. The latter transition in some cases is accompanied by the occurrence of lipidic particles as detected by freeze-fracturing. Thus, specific 13C-labeling experiments allow the study of the individual phase behaviour of lipids in mixed lipid systems. 3. In diet experiments using rats, the choline group of phosphatidylcholine present in erythrocyte, endoplasmic and sarcoplasmic reticulum membranes could be specifically 13C-labeled. The 13C line-widths of the resonance from the erythrocyte are typical for a lamellar arrangement of the membrane lipids. In strong contrast, the line-width observed at 37 degree C for the endoplasmic and sarcoplasmic reticulum membranes is much smaller, typical of the isotropic phases observed in model membranes. In isolated rat liver microsomes and liver slices, the 13C line-width is strongly temperature dependent. At lower temperatures the line-widths strongly increase towards values typical of lipids in a bilayer structure.

Animals↗