Low Choline Diet Research Articles

Influence of estradiol on apparent phosphatidyl choline synthesis in rats

SUMMARY Oophorcctomized Sprague-Dawley rats, 28 to 30 days old, were maintained for 31 days on either a normal diet or a high fat, low protein, low choline diet, with or without vitamin BIZ. Twice weekly injections of sesame oil or estradiol in sesame oil were administered subcutaneously. The animals kept on the high fat, low choline diet showed severe fatty metamorphosis of the liver, a decreased hepatic lecithin concentration, and a twofold increase in the relative specific activity of lecithin. Estradiol inhibited fatty metamorphosis and increased the lecithin concentration slightly. The animals receiving a vitamin Blrsupplemented diet and estradiol showed the greatest lipotropic effect and an increased liver lecithin concentration. Estradiol alone, or combined with vitamin B,?, did not correct the apparent choline deficiency, as meaaued by the abnormally high rate of P32 incorporation into lecithin. The results suggest, therefore, that the prevention of fatty livers by estradiol depends on mechanisms other than those involved in the lipotropic properties of choline or vitamin B12.

Ethanolamine on choline deficiency in rats

The addition of ethanolamine to low choline diets containing either 18 or 42% casein increased the incidence of both hemorrhagic kidneys and hemorrhagic eyes in weanling male rats consuming these diets for 7 days. At the same time the accumulation of liver fat in all animals was prevented by the added ethanolamine. The addition of 2-amino-2-methyl-1-propanol increased the severity of the hemorrhagic condition both in the presence and in the absence of ethanolamine. Animals consuming 42% casein diets were affected less severely by ethanolamine. When choline was added to the diets containing added ethanolamine, kidney and eye hemorrhages did not occur.

The Influence of Diet upon the Storage of Vitamin B12 in Liver and Kidney

Litter mate weanling rats were depleted for two weeks of vitamin B12 and either riboflavin, folic acid or choline. For a 4-week experimental period they were injected with 1.5 µg of vitamin B12 weekly and fed either a diet low in one of the vitamins being studied (0.2 mg riboflavin, or 0.1 mg folic acid or 0.05 gm choline per 100 gm of diet) or the same diet with a high level of the vitamin (1.0 mg riboflavin, 0.5 mg folic acid, or 0.1 gm choline per 100 gm). The vitamin B12 content of the lyophilized livers and kidneys was determined, using the Z strain of E. gracilis with respect to both total and free vitamin. Littermates were continued for the additional 4-week period on the deficient diet. For all three vitamins the deficient rats showed a significantly lower level of both total and free vitamin B12. The dietary increase of riboflavin or of folic acid from low to higher levels resulted in small increases of total and free vitamin B12 in both liver and kidney on a dry weight and on a nitrogen basis. There was evidence of interrelationship. On the high-riboflavin diet the free vitamin B12 increased to 100% in the liver and remained at 80% in the kidney. On the high-folic acid diet the free vitamin B12 remained close to 80% in the liver and 100% in the kidney. While the vitamin B12 content of the low-choline diet approximated those for the two other low diets, the high diet showed a significant decrease which could not be accounted for by possible lesions produced during the depletion period. The free vitamin B12 dropped from 91 to 77% in the liver and remained at 100% in the kidney. The storage of vitamin B12 in liver and kidney was influenced not only by the vitamin B12 content of the diet but by constituents such as riboflavin, folic acid and choline at levels below optimal but sufficiently high to prevent deficiency symptoms.

ANURIA DUE TO CARBON TETRACHLORIDE INTOXICATION

Article1 June 1958ANURIA DUE TO CARBON TETRACHLORIDE INTOXICATIONWARREN R. GUILD, M.D., JOHN V. YOUNG, M.D., JOHN P. MERRILL, M.D., F.A.C.P.WARREN R. GUILD, M.D.Search for more papers by this author, JOHN V. YOUNG, M.D.Search for more papers by this author, JOHN P. MERRILL, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-48-6-1221 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONThere are many drugs and chemicals which can produce renal injury resulting in acute urinary suppression. Among these is carbon tetrachloride,1, 2 which is widely used as an industrial solvent, as a household cleanser, as a vermifuge, and as a constituent of some types of fire extinguishers. This report is a clinical analysis of 20 patients with anuria due to carbon tetrachloride intoxication seen at the Peter Bent Brigham Hospital between 1948 and 1957.RESULTSOf the 20 cases, 16 were male and four were female. Their ages varied from 23 to 49 years. There were five deaths, or...Bibliography1. Smetana H: Nephrosis due to carbon tetrachloride, Arch. Int. Med. 63: 760-777, 1939. CrossrefGoogle Scholar2. Sirota JH: Carbon tetrachloride poisoning in man, J. Clin. Investigation 28: 1412-1422, 1949. CrossrefMedlineGoogle Scholar3. Von Oettingen WF: The halogenated hydrocarbons: toxicity and potential dangers, U. S. Public Health Publication No. 414, Washington, 1955. Google Scholar4. Vallee BL: Personal communication. Google Scholar5. GriffithWade WHNJ: The occurrence and prevention of hemorrhagic degeneration in young rats on a low choline diet, J. Biol. Chem. 131: 567, 1939. CrossrefGoogle Scholar6. Hartroff WS: Pathogenesis of renal lesions in weanling and young adult rats fed choline deficient diet, Brit. J. Exper. Path. 29: 483, 1948. Google Scholar7. KatskinKrehl GWA: The effect of alcohol on the choline requirement. II. Incidence of renal necrosis in weanling rats following short term ingestion of alcohol, J. Exper. Med. 100: 615-627, 1954. MedlineGoogle Scholar8. Takasaka T: Ueber die Lungenblutungen bei der akuten Tetrachlormethanvergiftung, Deutsche Ztschr. f. d. ges. gerichtl. Med. 6: 488, 1925. Google Scholar9. Merrill JP: The treatment of renal failure, 1955, Grune and Stratton, New York. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Boston, Massachusetts*Received for publication March 27, 1957.From the Department of Medicine, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Massachusetts.This study was supported in part by grants from the Medical Research and Development Board, Office of the Surgeon General, Department of the Army, the U. S. Public Health Service, the American Heart Association, and the Massachusetts Heart Association.Requests for reprints should be addressed to Warren R. Guild, M.D., Peter Bent Brigham Hospital, 721 Huntington Avenue, Boston 15, Massachusetts. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByAliphatic Halogenated Hydrocarbons: Report and Analysis of Liver Injury in 60 PatientsEffects of human Umbilical Cord Stem Cells and Granulocyte Colony- Stimulating Factor (G-CSF) on Carbon Tetrachloride-Induced NephrotoxicityHalogenated HydrocarbonsFatal Accidental Ingestion of Carbon Tetrachloride: A Postmortem Distribution StudyPost-Mortem Distribution and Histologic Study on a Fatal Case due to Accidental Ingestion of Carbon TetrachlorideInteraction of Ethanol with Other DrugsHepatotoxicity of AlcoholMetabolism of ethanol and associated hepatotoxicityToxic NephropathiesThe role of metabolism in carbon tetrachloride-mediated immunosuppression: In vivo studiesMechanism of ethanol induced hepatic injuryMinnesota highway maintenance worker cohort mortality study: Methods and noncancer mortalityEffects of Alcohol on Other HepatotoxinsIncreased urinary enzyme excretion in workers exposed to nephrotoxic chemicalsSentinel Health Events (Occupational): A Basis for Physician Recognition and Public Health SurveillanceTherapy of Toxic NephropathiesChemically Induced Nephrotoxicity: Role of Metabolic ActivationEffect of CO2-induced hyperventilation on carbon tetrachloride (CCl4) levels following acute CCl4 poisoningSentinel Health Events (occupational): a basis for physician recognition and public health surveillance.Early indicators of renal damage in workers exposed to organic solventsEffect of an acute dose of ethanol on the hepatotoxicity due to carbon tetrachlorideApplication and Results of Whole-Body Autoradiography in Distribution Studies of Organic SolventsChloroform: A Review of Its Metabolism, Teratogenic, Mutagenic, and Carcinogenic PotentialOn the differential diagnosis of acute renal failureThe Dangers from Limited Exposure to Carbon TetrachlorideEnhanced hepatotoxicity of carbon tetrachloride, thioacetamide, and dimethylnitrosamine by pretreatment of rats with ethanol and some comparisons with potentiation by isopropanolPotentiation of carbon tetrachloride hepatotoxicity by ethanol and coldSuicid durch einmalige Inhalation von Tetrachlorkohlenstoff (CCl4) mit LeukoencephalopathieAkutes NierenversagenBegutachtung der NierenerkrankungenRelative effects of various chlorinated hydrocarbons on liver and kidney function in miceIndications for DialysisToxic nephropathyAcute Renal Failure Due to Carbon Tetrachloride PoisoningRelative nephrotoxic properties of chlorinated methane, ethane, and ethylene derivatives in miceCARBON TETRACHLORIDE POISONING: A CASE REPORT AND REVIEWAcute Renal Failure Due to Tubular NecrosisSelected electrocardiographic changes during acute renal failure and hemodialysisPROBLEMS IN THE MANAGEMENT OF ACUTE RENAL FAILUREAcute Tubular Necrosis Report of a Case with Failure to Recover after Sixty-seven Days of OliguriaPETER A. F. MORRIN, M.B., B.CH., W. BURTON GEDNEY, M.D., WERNER BARTH, M.D., R. H. HEPTINSTALL, M.D. 1 June 1958Volume 48, Issue 6Page: 1221-1227KeywordsHeartHospital medicineIngestionIntoxicationMedical servicesNauseaNecrosisPneumoniaSurgeonsTetrachloride Issue Published: 1 June 1958 PDF DownloadLoading ...

Betaine and methionine on renal hemorrhagic degeneration in rats receiving 2-amino-2-methyl propanol-1.

Summary1. The incidence of hemorrhagic kidneys in young male rats on a low choline diet is increaased by the addition of 10 mg of 2-amino-2-methylpropanol-l per gram of food. Choline at a level of 10.76 × 10−3 mM per gram of food protects against renal hemorrhagic degeneration caused by 10 mg of 2-amino-2-methylpropanol-l per gram of food. Betaine, methionine, and casein at the levels studied were unable to completely prevent the incidence of kidney lesions caused by 10 mg of 2-amino-2-methylpropanol-l per gram of food.

Atheromatous changes in aorta, carotid and coronary arteries of choline-deficient rats.

Lesions have been observed in the aortas, carotid and coronary arteries in 26 of 116 rats fed a low choline diet for periods up to 216 days. None of these animals exceeded 300 days of age at the time of sacrifice. The initial lesion consists microscopically of the deposition of stainable lipid in the endothelial cells of the intima. In later stages, a proliferation of intimal cells had taken place so that small plaques resulted. In the large vessels (aortas and carotids) the subjacent media had undergone necrosis and eventual calcification. The possible relation of these lesions to atheroma in man is discussed.

Electrophoretic Studies on Serum and Plasma of Control and Vitamin Deficient Monkeys.

SummaryThe plasma or serum proteins of rhesus monkeys maintained on various vitamin deficient diets were studied by chemical and by electrophoretic analysis. Partial or complete deficiency of vit. B6 resulted in hypoalbuminemia and a significant increase in the gamma globulin component. On a niacin deficient diet 2 monkeys developed a lowered albumin and an increase in the gamma globulin. A low choline diet led to a decrease in the albumin and to an increase in the beta globulin. The addition of 1% cholesterol to the diet of control or vit. B6 deficient monkeys produced a significant increase in the alpha-3 component. The electrophoretic composition of the plasma did not appear to be altered by a state of early chronic scurvy. The mobilities of the plasma components appeared to be increased by an ascorbic acid deficient diet but were unaffected by the other regimens.

The effect of sex hormones on hepatic and renal lesions induced in rats by a choline-deficient diet.

While producing cirrhosis in rats by high fat, low choline diets, the authors observed that the livers of female rats showed less severe lesions than those of males. Similarly, the kidneys of young females appeared to withstand the effects of low choline diets better than the kidneys of young males. These findings are in agreement with those first reported by Griffith (1940). In an effort to explore the factors involved in these sex related differences, injections of estrogens and androgens were given to groups of both males and females on the experimental diet. The results indicate that the renal and hepatic lesions which develop after feeding rats a high fat, low choline diet may be altered by hormonal injections. The present findings, plus those reported in a preliminary note (1947) complement the work of Gyorgy, Rose, and Shipley (1947, 1949).

Choline Metabolism: VIII. The Relation of Cystine and of Methionine to the Requirement of Choline in Young Rats

Supplementary cystine (0.1 to 0.2%) or methionine improves the growth and efficiency of utilization of food in young rats on an 18% casein diet. The deposition of liver fat and the incidence of renal hemorrhagic degeneration in young rats on a low choline diet are increased by supplements of cystine (0.1 to 0.2%) which improve the nutritive value of the diet. Larger supplements of cystine have no effect on the requirement of choline. In the absence of dietary choline, 30% of casein is required to supply sufficient methionine and cystine for the prevention of signs of choline and cystine deficiency. Evidence is presented for the conclusion that methionine which is needed and used as a source of labile methyl is not utilizable as a source of cystine sulphur.

Choline Metabolism: IV. The Relation of the Age, Weight and Sex of Young Rats to the Occurrence of Hemorrhagic Degeneration on a Low Choline Diet, One Figure

Hemorrhagic degeneration occurred within 10 days in male rats, 20 to 30 days of age, on a low choline diet containing 0.3% of added cystine. A marked decrease in the incidence of the deficiency in similar rats, 33 days of age or older, suggested that there is a corresponding decrease in the choline requirement of rats over 30 days of age. The renal lesions in 40-gm. male rats, 21 to 26 days of age, were most severe on the sixth and seventh days. Only 60 to 80% of these rats survived the 10-day period. The results of choline deficiency appeared more slowly and were less severe in young female rats than in male rats of the same age and weight. The administration of choline after the appearance of hemorrhagic degeneration accelerated the recovery from the acute stage of the deficiency. The increase in weight of the kidneys of male rats, 20 days of age and 24 to 30 gm. in weight, after a 7-day period on diets containing suboptimal levels of added choline was proportional to the severity of the deficiency of choline.

Relation of Methionine, Cystine and Choline to Renal Lesions Occurring on Low Choline Diets

In a previous report1 it was demonstrated that a severe pathological state characterized by hemorrhagic degeneration of the kidneys occurs within 10 days in young rats maintained on a low choline diet. This deficiency was prevented by choline. It was suggested that proteins relatively high in methionine and low in cystine possessed a choline-sparing action since the deficiency was produced more readily on diets containing fibrin than on those containing casein. Subsequent work has confirmed the earlier suggestion that choline might prevent the renal lesion resulting from the addition of cystine to a purified diet containing casein. Furthermore, it has been found that the addition of methionine to a diet containing fibrin completely protected the rats.Normal kidneys were found in 40 g rats fed the following diet for 10 days: casein, 15; salt mixture, 4; calcium carbonate, 1; codliver oil, 5; lard, 35; agar, 2; sucrose, 32, and yeast, 6. Hemorrhagic kidneys invariably occurred if 0.3% cystine was added but ...

Some Effects of Low Choline Diets

The importance of choline in the prevention of “fatty livers” has been previously demonstrated by the investigations of Best1 and of Channon.1 The following experiments indicate that the production of a fatty liver on a low choline diet is only one manifestation of a more fundamental deficiency condition.Male rats, 40 g in weight and 24 days of age, were used in groups of ten. The basal diet consisted of fibrin-4, casein-8, dried egg white-3, salt mixture2-4, calcium carbonate-1, codliver oil-5, lard-35, agar-2, and sucrose-38. The water soluble vitamins were supplied by a daily supplement of 0.02 mg of thiamin chloride, 0.02 mg of riboflavin, 0.04 mg of nicotinic acid and 0.1 cc each of concentrated extracts of rice polish and hog liver. The rats consumed 4 to 5 g of food per day. The term fatty liver refers in every case to enlarged livers containing from 8 to 12 times the normal weight of chloroform-soluble substances.This newly recognized effect of choline deficiency was brought to light when rats wer...

Influence of a Pancreas Extract and Other Proteins on Liver Fat and Ketosis

SummaryAlthough they do not offer direct proof our experiments support the view that the reduction in liver fat caused by the pancreas extract which Dragstedt has described as lipocaic is due to the sum of the lipotropic effects of the choline and protein which it contains. The influence of the pancreas extract upon the fat content of the livers of rats on a low protein and low choline but high fat diet is greater than that of a similar amount of protein in other forms. The ketosis which results when rats with such fatty livers are fasting is reduced about equally by the pancreas extract and an equivalent amount of casein. Althought both the choline and the protein contained in the pancreas extract affect the fat content of the liver, choline is without antiketogenic activity under the conditions studied here.