Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By morphometric analysis of fatty liver, we propose to value volume density of fat vacuoles and liver hypertrophy. By this method we appreciate liver cell modification in malnutrition.
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PMID:[Morphometric study of hepatocytes in steatosis]. 390 76

Ibuprofen is a 2-arylpropionic acid anti-inflammatory agent that undergoes stereoselective chiral inversion (R to S configuration) as well as oxidative metabolism in humans and rats. The present study was undertaken to define more clearly the role of the liver in ibuprofen stereoisomer clearance in both normal and disease states. Liver perfusion experiments were conducted with normal and fatty rat liver; chronic fatty liver was induced by nutritional deficiency and was used as a model of hepatotoxin-induced fatty liver in humans. Total (R)-ibuprofen clearance (ClRtot), chiral inversion-related clearance (ClRinv), (S)-ibuprofen clearance (ClS) and hepatic distribution coefficients for each stereoisomer (KR and KS) were calculated with a model that corrected for perfusate reservoir sampling. In both normal and fatty liver, ClRinv accounted for 60% of ClRtot, but ClRtot was 30% lower in fatty liver than in normal liver (P less than .001). ClS was 40% of ClRtot in normal liver and was not significantly different from the noninversion clearance of (R)-ibuprofen. ClS was unchanged between normal and fatty liver and KS was greater than KR in normal liver (P = .01) but not in fatty liver. The results indicate that the fatty liver condition stereoselectively affects (R)-ibuprofen clearance and eliminates preferential (S)-isomer hepatic distribution. Based on model simulations, these effects are predicted to have minimal impact on total ibuprofen plasma levels or area-under-curve measurements following a dose of rac-ibuprofen unless ClRtot is reduced by more than 50%.
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PMID:Ibuprofen stereoisomer hepatic clearance and distribution in normal and fatty in situ perfused rat liver. 397 21

To determine if NMR techniques might be used to detect hepatic steatosis secondary to protein malnutrition, the T1 and T2 relaxation times of liver tissue from rats subjected to long-term protein malnutrition were measured in vitro. The liver tissue from rats fed a protein-deficient rat chow (PD) for 37 days (N = 9) was characterized by increased proportion of fat (P less than 0.001) but decreased water and nitrogen contents (P less than 0.001) relative to controls (N = 9). Mean T1 times were significantly shorter and T2 times significantly longer in liver tissue from protein-depleted animals (P less than 0.001). There was no overlap of T2 times between the protein-depleted and control animals. The consistent changes in T2 that occur with fatty infiltration of the liver should be detectable by current NMR imagers.
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PMID:In vitro detection of fatty liver infiltration in protein-depleted rats using proton nuclear magnetic resonance. 401 Feb 73

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.
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PMID:Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy. 430 60

Experimental protein-calorie malnutrition was produced in rats by feeding them a low-protein diet for 6 weeks. Control animals were fed a high-protein diet. The deficient rats showed severe restriction of body weight gain, fatty liver and hypoproteinemia. In addition the present study demonstrated that the experimentally-induced protein-calorie malnutrition brings about striking pathological and electrocardiographic changes as well as increased cardiac catecholamine levels. Based on this demonstration and considering the synchronism of morphological, electrophysiological and biochemical data, we postulated that nutritional stress to the heart raises the myocardium norepinephrine concentration, and continued exposure to high levels of catecholamines may play a role in the development of cardiac changes in protein-energy malnutrition.
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PMID:The heart in protein-calorie malnutrition in rats: morphological, electrophysiological and biochemical changes. 677 57

Experimental protein-calorie malnutrition was produced in rats by giving them a low-protein diet for 6 weeks. Control animals were fed a high-protein diet. The deficient rats showed severe restriction of body weight gain, fatty liver and hypoproteinaemia. In addition the present study demonstrates that the experimentally induced protein-calorie malnutrition brings about marked pathological changes and increased catecholamine levels in the hearts of rats. Based on this demonstration, and considering the synchronism of morphological and biochemical data, we postulate that the nutritional stress to the heart raises the myocardium noradrenaline concentration and the continued exposure to high levels of catecholamines may play a role in the development of cardiac changes in protein-energy malnutrition.
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PMID:Noradrenaline levels and morphologic alterations of myocardium in experimental protein-calorie malnutrition. 678 Jun 72

In this investigation, the ultrastructural features of the nutritional cardiomyopathy of protein-calorie-malnourished rats were examined. Protein-calorie malnutrition was induced in young rats by feeding them a low-protein diet (4% protein) for 6 weeks. Control animals were fed a high-protein diet (16% protein). The deficient rats showed severe restriction of body-weight gain, fatty liver and hypoproteinaemia. The results of the present study clearly demonstrated that the experimentally induced protein-calorie malnutrition brings about striking morphological changes in the heart of the rat. On light microscopy hyalinization an vacuolization of muscle fibres, loss of cross striations and myofibrils, small foci of necrosis, interstitial fibrosis and mononuclear-cell infiltration could be detected. The ultrastructural lesions were characterized by myofibrillar degeneration, contraction-band formation, dilatation of sarcoplasmic reticulum, mitochondrial swelling, dehiscence of intercalated discs, and widened interstitial spaces, especially around vessels, due to oedema fluid and cellular infiltration by mononuclear cells an activated fibroblasts with collagen fibres and microfibrils. In addition, an increase in relative heart weight was also observed. The potential role of catecholamines in the pathogenesis of this cardiomyopathy is discussed.
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PMID:Ultrastructural changes in nutritional cardiomyopathy of protein-calorie malnourished rats. 680 35

Development of alcohol-related liver and other diseases appears to be modified by host and environmental factors that include diet and nutritional status, exposure to other drugs and toxins, and infection. The relative importance of alcohol toxicity and malnutrition in the induction of fatty liver and cirrhosis, the subject of this report, has been debated. Male rhesus (M mulatta) monkeys were fed purified liquid diets, adequate or marginally deficient in lipotropes (choline, methionine, and folate), containing ethanol to supply 40-50% of calories for 1.5-4.5 years. Controls, fed the diets with sucrose and fat isocalorically substituted for ethanol, grew well and were clinically normal. Ethanol-fed monkeys in both diet groups failed to gain weight and were slightly anemic, with mild derangements of serum electrolytes and small amounts of fat in their livers. None had fibrosis or cirrhosis until the severity of the lipotrope-deficiency was increased; then two of four deficient animals developed cirrhosis and one developed fibrosis. (The severe deficiency induced weight loss and fatty liver, but not fibrosis, in one of two controls.) We conclude that alcohol does not induce hepatic fibrosis or cirrhosis in rhesus monkeys fed a nutritionally complete diet, a result supported by studies in rats and another monkey, M radiata. Alcohol does induce cirrhosis when fed in combination with a lipotrope-deficient diet that is not, by itself, cirrhogenic.
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PMID:Ethanol and diet interactions in male rhesus monkeys. 692 13

Ten patients with fatty liver, distinct from the well known diffuse alcoholic variety, comprise this report. All patients had an initial ultrasound examination followed by 99mTc-sulfur colloid liver and computed tomography (CT) body scans. Six patients had focal fatty infiltration producing a space-occupying mass within the liver. Four had ultrasound evidence of diffuse fat occurring in association with focal masses. These masses were all echo poor relative to the adjacent fat, and were subsequently found to represent nodules of normal uninvolved liver in two patients, and metastatic neoplasm and multiple liver cysts in single patients respectively. The clinical picture associated with fatty liver is variable and may include, in addition to alcohol abuse, obesity, malnutrition, exogenous glucocorticoids, diabetes mellitus, and other less well defined factors. Dramatic improvement in fatty liver occurred in two patients following appropriate therapy. The spectrum of changes produced by fatty infiltration of the liver on ultrasonic, radionuclide, and CT scans is extremely varied depending on the amount of fat deposition, its focal or generalized nature, and the presence of associated liver disease.
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PMID:Fatty infiltration of the liver--an imaging challenge. 716

To evaluate possible effects of alcohol consumption on vitamin A and retinol-binding protein (RBP) status, baboons were pair-fed a nutritionally adequate liquid diet containing 50% of total calories either as ethanol or isocaloric carbohydrate. Fatty liver developed after 4 months of ethanol feeding with a 59% decrease (P less than 0.001) in hepatic vitamin A levels, and fibrosis or cirrhosis developed after 24-84 months with a 95% decrease (P less than 0.001). Similarly, hepatic vitamin A levels of rats fed ethanol (36% of total calories) were decreased after 3 weeks (42%, P less than 0.01) and continued to decrease up to 9 weeks. In contrast, vitamin A contents in the kidney and testis were increase 2-3 fold in ethanol-fed rats after 9 weeks. Serum vitamin A and RBP levels were not significantly changed in rats. When dietary vitamin A was increased 5-fold, hepatic vitamin A was again decreased in ethanol-fed rats. When dietary vitamin A was virtually eliminated, the depletion rate of vitamin A from endogenous hepatic storage was 2.5 times faster in ethanol-fed rats than in controls. It is concluded that chronic ethanol consumption decreases hepatic vitamin A, and that some mechanisms other than malnutrition and malabsorption may be involved in this process.
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PMID:Hepatic vitamin A depletion after chronic ethanol consumption in baboons and rats. 719 10


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