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)

Serum zinc and copper levels were studied in relation to in vitro and in vivo drug metabolism in 25 alcoholics, in whom various diseases of the liver had been diagnosed by histology. Serum zinc was elevated in alcoholics with normal or fatty liver and was low in those with alcoholic hepatitis or cirrhosis. There was a significant positive correlation between serum zinc and cytochrome P-450 content of liver biopsies. The relationship between zinc and antipyrine half-life was significant and non-linear. Serum copper level was elevated in all the alcoholics and no significant relationship could be found between copper and drug metabolism in alcoholics. The findings suggest parallelism between changes in serum zinc and indices of drug metabolism in alcoholics.
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PMID:Serum zinc and serum copper and indices of drug metabolism in alcoholics. 92 28

Most of the common breakfast cereals tested were unable to support growth or promote health in young rats that consumed these products as their only food. An anemia, accompanied by fatty liver and large concentrations of iron stored in the liver, was observed with cereals having the lowest protein content. Some cereals produced a marked elevation of systolic blood pressure at certain times. Low cholesterol levels were invariably associated with fatty livers, whereas high cholesterol levels seemed to be associated with hypertension at the 45-day period. When only the ready-to-eat cereals were considered, there was a positive correlation between the dietary zinc/copper ratio and the plasma cholesterol concentration.
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PMID:Growth, hemoglobin, cholesterol, and blood pressure observed in rats fed common breakfast cereals. 126 94

In 20 cases of total pancreatectomy and 74 cases of pancreaticoduodenectomy, pancreatic endocrine and exocrine functions in long-term survival after surgery were investigated, particularly in relation to development of fatty liver, metabolic bone disorder and changes of serum zinc. In cases of pancreaticoduodenectomy, although the residual pancreatic endocrine and exocrine functions decreased in 1 or 2 months, they were recovered within a year and these functions were maintained relatively well, but in cases of resection of fibrotic pancreas, they decreased gradually in more than 3 years after surgery. In a long-term survival, fatty liver, metabolic bone disorder and an impaired absorption of zinc developed, and such changes occurred remarkably in cases of resection of fibrotic pancreas or in cases of total pancreatectomy. Hence, after major resection of the pancreas, a long-term sufficient control should be necessary understanding these pathophysiology.
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PMID:[Pathophysiology during follow-up after extensive pancreatectomy]. 322 97

Alcohol has at least two actions on essential fatty acid (EFA) and Prostaglandin (PG) metabolism. It enhances the conversion of dihomogammalinolenic acid (DGLA) to PGE1 but it blocks the activity of the delta-6-desaturase, an enzyme necessary for replenishment of DGLA stores from dietary precursors. The acute effect of ethanol is therefore an increased production of PGE1 but chronic consumption will lead to depletion of DGLA and PGE1. Withdrawal from alcohol will lead to a precipitous fall in PGE1. PGE1 is known to have profound effects on the nervous system and behaviour. Patients with mania produce more PGE1 than normal while those with depression make less. Alcoholics may drink to maintain a normal PGE1 level, something which will require more and more ethanol as DGLA is depleted. In both animals and humans PGE1 or its precursor, gamma-linolenic acid (GLA) have been shown to attenuate the acute withdrawal syndrome. PGE1 injections prevent the development of fatty liver in alcohol-treated animals. Defective EFA and PGE1 metabolism are known to lead to increased fibrosis, reproductive failure, cardiomyopathy, cardiovascular disorders, gastritis and pancreatitis and could therefore be the basis for these disorders in alcoholics. A PGE1 deficiency could also be responsible for the fetal alcohol syndrome. Three other agents are known to produce constellations of fetal defects very similar to those found in the alcohol syndrome. These other factors are dihphenylhydantoin, lithium, and a deficiency of zinc. These three factors and excessive alcohol consumption all lead to PGE1 deficiency by different routes. If this concept is correct, the key to the management of alcoholism and its medical complications lies in the provision of GLA or DGLA, fatty acids which by-pass the alcohol blocked step and which are unfortunately unlikely to be present in any normal diet. Unlike many concepts of alcoholism and alcohol damage, the EFA/PGE1 idea is very readily testable and already has considerable experimental support.
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PMID:A biochemical basis for alcoholism and alcohol-induced damage including the fetal alcohol syndrome and cirrhosis: interference with essential fatty acid and prostaglandin metabolism. 625 73

Four groups of 6 rabbits were subjected to the following diets for 25 weeks: I (controls), II (water with 9.66 mumol/l of lead), III (atherogenic) and IV (atherogenic + 9.66 mumol/l of lead). Lead, magnesium, calcium, zinc and cadmium were then analyzed in 20 dry tissues. At the level of the arteries, veins and skin a tendency was observed toward increased lead concentration in rabbits of groups II and IV, elevated calcium levels in groups III and IV (a tenfold increase of calcium in the aortas), and a higher concentration of cadmium in animals of group II. There was a significant reduction in lead and magnesium concentrations in the liver of animals in groups III and IV because of fibrosis and overabundance of fatty liver cells. The lead level in the liver of animals in group II had slightly increased. Lead concentrations were higher in the kidneys and spleen in groups II and IV. Cadmium levels were significantly lower in the liver, kidneys, adrenal glands and spleen of animals in groups III and IV, whereas in group II they were particularly increased in the liver and kidneys. Very little significant interaction between the two diets was noted. Rabbits in groups III and IV showed notable histopathological alterations in aorta, carotid and femoral arteries, left ventricle and liver. Extrapolation from rabbit to man would be inadvisable.
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PMID:Concentrations of lead, magnesium, calcium, zinc and cadmium in twenty rabbit tissues after exposure to low lead doses and atherogenic diet. 665 Dec 30

Serial liver biopsies were carried out in 67 patients with HLP and/or fatty liver before, during short- and long-term therapy with CPIB and after termination of therapy. Results (1) Decrease of liver glycogen from 4.17% to 2.69% (wet weight, P less than 0.02). (2) Insignificant changes of liver triglyceride content. (3) Significant decrease of manganese, while the concentrations of zinc and copper in the liver biopsy specimens remained unchanged. (4) No signs of liver intoxication or cancerogeneous effects of light-microscopic pictures. (5) Significant increases in numbers of mitochondria and cristae as well as a hypertrophy of endoplasmic reticulum with longer lasting therapy. (6) Striking focal proliferation of cristae mitochondriales in 3 cases on longterm treatment. (7) Regression of the mitochondrial alterations after termination of the CPIB therapy. Our findings suggest that an increased number of mitochondria and of their inner membranes in the liver cells induced by CPIB could play an important role in the hypolipidemic action of the drug.
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PMID:Effects of p-chlorophenoxyisobutyric acid (CPIB) on the human liver. 740 47

In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver, whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) ("coconut oil diet") or linseed oil (80 g/kg) ("linseed oil diet") as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Zinc deficiency and activities of lipogenic and glycolytic enzymes in liver of rats fed coconut oil or linseed oil. 776 Jun 90

In the present work the influence of zinc deficiency on fat content and fatty acid composition of liver and fatty acid composition of brain of rats with a high food intake was investigated. Using the force-feeding technique the rats were fed 14.5 g food daily at days 1 to 4, and then 11.6 g food for later days. After 7 days the zinc-deficient animals had a fatty liver which was characterized by an increase in fat content (68%) and dry matter (23%). The amounts of lauric acid, myristic acid, myristoleic acid, palmitic acid, palmitoleic acid, and oleic acid were also increased by 100 to 200% in the liver of zinc-deficient animals, whereas the amount of arachidonic acid was decreased by 29%. The amounts of phosphatidylcholine and phosphatidylethanolamine in the liver were not changed by zinc deficiency, but the fatty acid composition of these phospholipids was changed. The liver phospholipids of zinc-deficient animals had a decreased proportion of arachidonic acid, but an increased proportion of docosahexaenoic acid. In the zinc-deficient animals there also existed a positive correlation between the fat content in the liver and the ratio between linoleic and arachidonic acid in the liver and a negative correlation between the fat content in the liver and the amount of arachidonic acid in the liver. These correlations as well as the changes in liver fatty acid composition of zinc-deficient animals suggest that the fatty liver might be the result of a disturbed metabolism of linoleic acid. In contrast, zinc deficiency did not influence the fatty acid composition of brain. This means that brain is protected against the effects of short-term zinc deficiency.
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PMID:[The effect of zinc depletion on the fat content and fatty acid composition of the liver and brain in forcibly fed rats]. 823 78

'Magnesium ischaemia' is a term used to denote the functional impairment of the ATP-dependent sodium/potassium and calcium pumps in the cell membranes and within the cell itself. The production of ATP and the functioning of these pumps is magnesium-dependent and is critically sensitive to acidosis. Zinc and iron deficiencies may secondarily impair these pumps and thus contribute to 'magnesium ischaemia' (as does acidosis). This term is two-dimensional at its simplest; it refers to a functional magnesium deficiency, whether actual or induced. It is argued that chronic acidosis is the most common inducing factor. This simple hypothesis can begin to unify diverse pathophysiologies: some spontaneous abortions, aspects of Type II and gestational diabetes and the curious observation that heroin addicts become diabetic. It can also unify clinical thinking about pregnancy-induced hypertension, pre-eclampsia/eclampsia and acute fatty liver of pregnancy, as well as the coagulopathy of pregnancy. It makes important predictions about perinatal morbidity and suggests that early supplementation might prevent much pregnancy-induced disease.
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PMID:The pathogenesis of eclampsia: the 'magnesium ischaemia' hypothesis. 839 28

Abnormal Zinc and Copper metabolism were studied in rats with tetracycline-induced fatty liver and compared with normal rats. The present work recorded decreased serum zinc concentration with increased copper concentration in the tetracycline-injected rats. The results also showed that the liver and heart zinc were significantly decreased; meanwhile it was observed that the concentration of zinc in the kidney tissue of fatty liver rats was significantly raised in comparison with those of normal rats. Histopathological studies of the kidney tissue showed degenerative changes in the tables with areas of focal necrosis. Renal tubular necrosis in such cases is largely caused by the toxic degradation products of tetracycline metabolism. The kidney lesion together with impaired gastrointestinal absorption contributed to the hypozincaemia observed in the present results. Although the present data showed a significant reduction in serum zinc and significant rise in plasma insulin in the fatty liver rats there was nonsignificant correlation between the two variables as compared with the normal rats. The positive correlation between serum zinc concentration and reduced high-density lipoprotein cholesterol (HDL-C) emphasizes the role of zinc deficiency in atherosclerotic disease in fatty liver.
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PMID:Abnormal zinc and copper metabolism in hepatic steatosis. 904 48


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