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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both epidemiological and experimental studies have demonstrated that a high content of n-3 fatty acids in the diet lowers serum lipid concentration. However, the mechanism for this effect is unclear. In this present study it has been shown that labelled linolenic acid (18:3, n-3) is oxidized to a larger extent than linoleic acid (18:2,n-6) in isolated rat hepatocytes. Conversely, the incorporation of linolenic acid and the desaturated/chain-elongated products in VLDL-triacylglycerol is decreased compared with linoleic acid. Dietary n-3 fatty acids have probably a depressing effect on both hepatic triacylglycerol synthesis and on secretion of VLDL. The finding that n-3 fatty acids are transported from the liver as ketone bodies to a larger extent than n-6 fatty acids may thus explain that a high intake of n-3 fatty acids is not accompanied with hepatic steatosis.
Scand J Clin Lab Invest 1988 Dec
PMID:Mechanisms for the serum lipid-lowering effect of n-3 fatty acids. 285 43

The reliability of proton spectroscopic imaging in evaluating fatty infiltration of the liver was investigated in 35 subjects (12 healthy volunteers and 23 patients with fatty livers). With this modified spin-echo technique, fatty liver could be separated from normal liver both visually and quantitatively. On the opposed image, normal liver had an intermediate signal intensity, greater than that of muscle, whereas fatty liver had a lower signal intensity, equal to or less than that of muscle. In normal livers, the lipid signal fraction was less than 10%, while in fatty livers it was greater than 10% and usually exceeded 20%. With this technique, nonuniform fatty infiltration of the liver can be differentiated from hepatic metastases, and the technique may prove useful in the differentiation of some hepatic disorders.
Radiology 1985 Dec
PMID:Fatty infiltration of the liver: evaluation by proton spectroscopic imaging. 299 37

The effects of ethanol administration on activity and regulation of carnitine palmitoyltransferase I (CPT-I) were studied in hepatocytes isolated from rats fed a liquid, high-fat diet containing 36% of total calories as ethanol or an isocaloric amount of sucrose. Cells were isolated at several time points in the course of a 5-week experimental period. Ethanol consumption markedly decreased CPT-I activity and increased enzyme sensitivity to inhibition by exogenously added malonyl-CoA. Changes in enzyme activity occurred sooner than those in enzyme sensitivity. Fatty acid oxidation to CO2 and ketone bodies was depressed in hepatocytes from ethanol-fed animals during the first part of the treatment. At the end of the 35-day period, there were no longer differences in the rate of ketogenesis between the two groups. At that time, however, the rate of CO2 formation was still impaired in the ethanol-fed animals. Furthermore, addition of ethanol or acetaldehyde to the incubation medium strongly depressed CPT-I activity and rates of fatty acid oxidation in hepatocytes from ethanol-treated rats, whereas these effects were much less pronounced in cells from control animals. The response of CPT-I activity to insulin, glucagon, vasopressin, and phorbol ester was blunted in cells derived from ethanol-fed rats. These changes in the regulation of CPT-I activity corresponded with those observed in the rate of fatty acid oxidation. It is concluded that CPT-I may play a role in the generation of the ethanol-induced fatty liver.
Arch Biochem Biophys 1988 Dec
PMID:Effects of ethanol feeding on the activity and regulation of hepatic carnitine palmitoyltransferase I. 306 12

Sixteen mongrel dogs were depancreatized and controlled with intravenous hyperalimentation that included fat emulsion (Intralipid) for four weeks. Plasma lipids, fat tolerance test, PHLA, and presence of fatty liver were investigated. Dogs were divided into three groups (A, B, and C) for the purpose of studying the effect of fat emulsion. Groups A(n = 6) and B(n = 5) were given fat emulsion 1g/kg/day and 2g/kg/day respectively. Group C(n = 5) was not given fat emulsion. Group B had increased plasma total cholesterol and phospholipid. Group A had a slight increase of TG only. Group C had decreased plasma total cholesterol and phospholipid, and became hypoglycemic sometimes. The ability to clear fat emulsion expressed as (K2) decreased significantly after the 14th day in group B only. LPL, determined by the PHLA test in groups B and C only, did not change significantly. It seemed that fat emulsion was utilized in part as FFA and ketone bodies. Infusion of fat emulsion did not lead to fatty liver when insulin was administered continuously. For the depancreatized condition, it appeared that fat emulsion could be useful when blood sugar was controlled with insulin.
Nihon Geka Gakkai Zasshi 1988 Dec
PMID:[Effect of intravenous administration of fat emulsion to depancreatized dogs]. 314 8

Ingestion of various liquid diets containing 36% calories as ethanol and 35% calories as fat does not provide adequate nutrition to young growing rats. Studies conducted with the aforementioned diets have the effects of malnutrition confounded with those of alcohol administration. Feeding a 26% alcohol liquid diet, which results in adequate nutrient intake with the same level of alcohol ingestion as the 36% alcohol diet, does not result in fatty liver development in the rat. The concept that prevailed for 25 years that fatty liver is caused despite adequate nutrition and hence is due to alcohol alone is therefore erroneous.
Med Hypotheses 1988 Dec
PMID:Is malnutrition necessary for the development of alcoholic fatty liver in the rat? 322 58

We describe 2 patients with biopsy-proven acute fatty liver of pregnancy in whom the diagnosis was suggested by the finding of uniform reduced attenuation values on computed tomography (CT) of the liver. The attenuation values returned to normal with resolution of signs and symptoms following delivery. CT of the liver provides a useful method for the diagnosis of acute fatty liver of pregnancy.
J Clin Gastroenterol 1988 Dec
PMID:The diagnosis of acute fatty liver of pregnancy by computed tomography. 323 Feb 82

1. Changes in lipid content and composition of liver and bile during pre- and post-laying periods were investigated in hens of a laying strain. 2. The large increase in liver lipid concentration, particularly triacylglycerols, at the onset of laying was accompanied by the appearance of triacylglycerols in the bile. 3. Accumulation of triacylglycerol in the liver was increased by a diet containing maize and soyabean meal. This was associated with increases in the triacylglycerol concentration in both serum and bile. 4. Liver microsomal phosphatidate phosphohydrolase activity was positively correlated with liver triacylglycerol content in birds given the maize/soyabean meal diet. 5. The time course of triacylglycerol accumulation in the liver and associated changes in the bile triacylglycerol concentration in laying strain hens were different to those previously observed in broiler hens. 6. Over the lifetime of the bird, secretion of triacylglycerols into bile may play an important role in the prevention of fatty liver syndromes.
Br Poult Sci 1987 Dec
PMID:Effects of age and diet on the lipid content and composition of gallbladder bile, liver and serum in laying strains of hen. 344 28

Percutaneous liver biopsy specimens were obtained from 11 control subjects, 24 alcoholic patients and six diabetic patients with mild to severe fatty liver and incubated in Krebs-Henseleit buffer containing 3H2O. The incorporation of 3H into fatty acid was measured and the absolute rate of fatty acid synthesis calculated. Fatty acid synthesis rates were significantly lower in alcoholic fatty liver than in controls. Fatty acid synthesis rates were similar in controls and patients with diabetic fatty livers. Addition of 50 mmol/l ethanol did not alter the fatty acid synthesis rates in vitro. It is concluded that enhanced lipogenesis is not the major cause of fatty liver in patients with alcoholic fatty liver.
Clin Sci (Lond) 1986 Dec
PMID:Fatty acid synthesis in vitro by liver tissue from control subjects and patients with alcoholic liver disease. 379 74

An experimental model for monitoring rat liver function during protracted exposure to hepatotoxic agents is proposed. Owing to their invasiveness, the models usually employed are appropriate for studying the mechanism of action of toxic substances, but do not allow the liver situation to be followed over the course of time. The need to sacrifice animals to determine liver triglycerides-one of the key parameters in the progress of toxic damage- reduces the possibility of following such progress in the same animals. This study describes the testing of a model for monitoring three basic parameters of liver injury: cytolysis, steatosis and metabolic deficiency of the liver. CCl4 has been chosen as model-hepatotoxin. Steatosis is determined by evaluating the triglyceride content of small specimens of liver, obtained through open-field biopsies, which appear to be representative of the whole liver. Fatty liver is paralleled by the block in Triton-induced hypertriglyceridaemia. Determination of serum triglycerides derives from a very poorly invasive technique which can be repeated several times. The combination of these tests with the assessment of both the cytolysis (ALT and SDH release into the circulation) and the impairment of the efficiency of liver microsomal enzymes (TMO clearance), seems to offer a reliable experimental procedure in predicting the hepatotoxic effect of xenobiotics.
Res Commun Chem Pathol Pharmacol 1986 Dec
PMID:A model for monitoring changes in liver function. 379 13

The authors report a further case of methimazole-associated liver damage and present a brief review of eleven previous cases found in the literature. The main clinical features of this 58-year-old female patient were laboratory evidence of leucopenia and cholestasis, and biopsy features of fatty liver parenchyma degeneration with granulocytic portal infiltration and bile stasis, demonstrated 20 days after the initiation of antithyroid therapy with 20 mg methimazole daily. An immediate cholestatic liver reaction was also provoked by drug rechallenge, with spontaneous amelioration of signs and symptoms after drug discontinuation.
Hepatogastroenterology 1986 Dec
PMID:Methimazole-associated cholestatic liver injury: case report and brief literature review. 380 81


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