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)

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below 0-8 mug/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0-35 mug/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.
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PMID:Fatty liver and kidney syndrome in chicks. II. Biochemical role of biotin. 1 36

Previous work in our laboratory and others suggests that protein malnutrition plays an important role in the pathogenesis of hepatic steatosis and dysfunction which characteristically appears after jejunoileal bypass for morbid obesity. Postoperative protein-calorie malnutrition is at least in part a consequence of diminished intestinal absorption of free amino acids. In an attempt to prevent liver disease, six morbidly obese patients were orally supplemented with essential amino acids for 4 months after surgery. Oral amino acid supplementation only partially influenced protein malnutrition and had no effect on deterioration of hepatic morphology and dysfunction. Although this mode of therapy appears to be ineffective in preventing postoperative liver abnormalities, other studies suggest that oral oligopeptide supplementation and parenteral administration of amino acids are beneficial. In addition to protein deificiency, other factors which may contribute to the development of liver disease are reviewed.
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PMID:Effect of oral amino acid supplementation on liver disease after jejunoileal bypass for morbid obesity. 40 55

In 40 obese patients, the liver function and the morphological picture were examined before and after jejuno-ileostomy. In 94% of the patients, distinct fatty liver was observed already before the small bowel exclusion, and the function tests showed an impaired function of this organ in 25% of the subjects before the operation. No clinical symptoms of liver insufficiency were recorded during the postoperative period. During one to three months after surgery, an increased impairment of the liver function was ascertained but, later on, a gradual improvement. More than one year after jejuno-ileostomy, the function test results were considerably better than before the operation. The degree of steatosis increased in the majority of the patients within 6 months after surgery, and some time later a considerable decrease in fatty liver was observed. Within 18 to 24 months after the jejunoileostomy, the morphological picture of the liver did not differe from the normal. The impaired function and the increased degree of steatosis were noted during diarrhea and rapid loss of body weight. The reson for this is most probably the protein malnutrition caused by the radical reduction in the absorption surface of the small bowel. The improved function and morphological picture of the liver are related to the progress of adaptation changes of the active part of small bowel. The results of the author's research do not confirm the hypothesis of permanent, harmful effect of jejuno-ileostomy on the state of the liver. The symptoms observed are definitely of a periodical and transient character, and are therefore not contra-indicated in the application of this operation in morbid extreme obesity treatment.
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PMID:Function and morphological picture of the liver in obese patients before and after jejunoileostomy. 74 72

In 15 mongrel dogs, a mixture of exocrine and endocrine pancreatic tissue obtained by a simple procedure was implanted into the liver of the same animal through a branch of the portal vein. Five animals with partial pancreatectomy were used for a morphological study. In a second group of ten dogs, 5 delayed and 5 immediate pancreatectomies were performed. No diabetes appeared after the pancreatectomy. The subsequent blood glucose and insulin levels remained within or close to the normal range for several weeks in 9 animals and up to 10 months in a last one, still alive. In 9 out of 10 animals, the long term study was limited between 6 and 17 weeks by the development of a malnutrition syndrome with hepatic steatosis due to the lack of exocrine secretory function because of the pancreatectomy. The last animal still alive developed the malnutrition syndrome after a second complementary resection of a small pancreatic fragment left along the duodenum. This last animal without diabetes at the 45th week suggests that the endocrine function of the autotransplanted pancreatic tissue could be maintained over a long period of time.
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PMID:[Prevention of diabetes in pancreatectomised dogs by autotransplantation of pancreatic tissue in the liver]. 81 64

The physical disease profiles of 135 female and 736 male inpatient alcoholics, similar in age, social class, and referral pattern, were compared to further clarify the widespread clinical impression that female alcoholics are more illness-prone. Although the women had been drinking hazardously for fewer years, at admission the prevalence of most diseases was similar in men and women. There was, however, an excess of anemia in women and of fatty liver and chronic obstructive lung disease in men. Furthermore, the average duration of hazardous drinking before the first recorded occurrence of almost all illness events was shorter in women, the sex differences being statistically significant for fatty liver, hypertension, obesity, anemia, malnutrition, gastrointestinal hemorrhage, and an ulcer requiring surgery. These findings suggest that the development of physical morbidity in relation to hazardous drinking may be accelerated in women.
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PMID:Morbidity in alcoholics. Evidence for accelerated development of physical disease in women. 87 27

Since 1964, 41 patients with strictly defined, severe primary (dietetic) protein malnutrition have been studied under metabolic ward conditions during prolonged periods, initially on a low (20 g) and later on a high (100 g) protein diet. Clinical, nutritional, hematological, intestinal absorptive and histological studies were performed in the malnourished state, during and after protein repletion. Classical signs and symptoms of malnutrition, lasting for at least 4 months, were present in most patients. Mild diarrhea was frequent. All were normoblastically anemic, hypoproteinemic, and hypocholesterolemic; serum folate values were normal or low but serum B12 values were normal or high. Liver biopsy showed fatty liver in the cases where it was performed. Mild malabsorption was detected in over one-half of the patients, with moderate intestinal radiological abnormalities. Malabsorption was independent of concomitant folate deficiency. All the clinical, absorptive and histological abnormalities reversed with treatment consisting only of a high protein diet. In addition to protein lack, another factor has to be invoked in the pathogenesis of the intestinal abnormalities present in severely malnourished adults from rural areas in the tropics.
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PMID:Enteropathy in adult protein malnutrition: a review of the Cali experience. 114 51

To study possible factors in the pathogenesis of the ethanol-induced fatty liver, we investigated the effect of chronic ethanol consumption on the metabolism of fatty acids by isolated hepatic mitochondria. Chronic ethanol consumption resulted in decreased fatty acid oxidation, as evidenced by a reduction in oxygen uptake and CO2 production associated with the oxidation of fatty acids. The State 3 rate of oxygen uptake was depressed to a greater extent than the State 4 or the uncoupler-stimulated rate; the respiratory control ratio was also decreased. Therefore, one site of action of chronic ethanol feeding is on oxidative phosphorylation. The reduction in fatty acid oxidation, in general, is not due to an effect on the activation or translocation of fatty acids into the mitochondria. There was no effect by ethanol feeding on the activity of palmitoyl coenzyme A synthetase, whereas carnitine palmitoyltransferase activity was increased. The use of an artificial system (formazan production) to study beta oxidation in the absence of the electron transport chain is described. In the presence of fluorocitrate, which inhibits citric acid cycle activity, ketogenesis and formazan production were increased by chronic ethanol consumption. Thus beta oxidation to the level of acetyl-CoA is not impaired by chronic ethanol consumption. Total oxidation of fatty acids to CO2 is depressed by chronic ethanol intoxication because of effects on oxidative phosphorylation or the citric acid cycle (or both). Neither nutritional deficiency, cofactor depletion, nor the presence of ethanol in vitro explains these effects. Several of the effects of chronic ethanol consumption on fatty acid oxidation are mimicked by acetaldehyde and acetate, products of ethanol oxidation. Chronic ethanol consumption leads to persistent impairment of mitochondrial oxidation of fatty acids to CO2. However, oxidation of fatty acids to acetyl-CoA is not decreased by chronic ethanol consumption.
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PMID:Effect of chronic ethanol ingestion on fatty acid oxidation by hepatic mitochondria. 117 Oct 98

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

Male weanling rats were fed a 72% rice diet containing no detectable carnitine and limiting in threonine and lysine. Such dietary conditions may simulate protein malnutrition in man. Under these conditions growth impairment, anemia, hypoproteinemia, and fatty liver developed. The study focused principally on the fatty liver syndrome which was corrected to varying extents depending on degrees of supplementation with carnitine, lysine, threonine, and appropriate combinations of these nutrients. Such reduction in fatty liver accumulation was accounted for principally by the lowering of triglycerides, but also in part of total cholesterol levels. All the data, which also included monitoring carnitine uptake by the tissues and measurement of plasma triglycerides, were consistent with the view that fatty liver accumulation occurs in amino acid deficient diets because (a) of an impairment in the synthesis of the lipoprotein complex mandatory for triglyceride secretion from the liver and (b) from a deficiency of carnitine needed for the intramitochondrial transport of fatty acids prerequisite for their oxidation.
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PMID:Dietary lysine and carnitine: relation to growth and fatty livers in rats. 124 84

The physical-disease charcteristics of 125 skid row and 736 non-skid row male alcoholics were compared in detail to determine whether skid row alcoholism is characterized by a distinct medical, as well as a social, profile. Trauma, tuberculosis, venereal disease, and malnutrition were more common in the skid row alcoholics. Epilepsy, peripheral neuritis, acute brain syndromes, chronic brain disease, and lifetime recordings of all nervous system illnesses also occurred more frequently in the skid row group, as did gastritis, gastrointestinal hemorrhage, ulcer surgery, and postgastrectomy syndrome. Fatty liver, hypertension, ischemic heart disease, cardiomyopathy, and cardiovascular illnesses of all kinds, however, were less common. The skid row medical profile is, in part, the product of a unique sociologic environment. Thus, skid row alcoholism may be viewed as a distinct sociomedical entity.
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PMID:Skid row alcoholism. A distinct sociomedical entity. 125 98


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