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

Serial studies of plasma lipids and lipoproteins were performed in 4 patients with acute alcoholic liver disease characterized by a massive fatty liver and laboratory evidence of intrahepatic cholestasis. There were striking alterations in the plasma lipoprotein electrophoretic patterns characterized by the absence of alpha- and pre-beta-lipoprotein bands and the presence of a single band of abnormal mobility. These changes were associated with an extreme decrease in plasma lecithin-cholesterol acyltransferase activity, resulting in greatly reduced levels of plasma cholesteryl esters and increased levels of unesterified cholesterol. In 2 patients hypertriglyceridemia and hypercholesterolemia were present, the latter because of an increase in unesterified cholesterol. Lipoproteins were isolated from the plasma by sequential ultracentrifugation at the densities used for separation of normal very low density, low density, and high density lipoproteins; however, the patients' lipoproteins were different from normal in lipid composition and ultrastructure. All of the lipoprotein fractions were decreased in cholesteryl esters and the major lipoprotein was a triglyceride-rich low density lipoprotein. Electron microscopic studies of the low and high density lipoprotein fractions revealed the presence of bilamellar vesicles and stacked discs. All of the changes in lipoprotein composition and ultrastructure gradually returned to normal with clinical improvement. These observations indicate that alcoholic liver injury is associated with profound alterations in lipoprotein composition and metabolism which may be related in part to lecithin-cholesterol acyltransferase deficiency.
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PMID:Abnormal plasma lipoproteins and lecithin-cholesterol acyltransferase deficiency in alcoholic liver disease. 18 10

Rats maintained on a high-fat diet supplemented with propylthiouracil develop a hypercholesterolemia, an increased serum level of apolipoprotein (apo) E, abnormal very low density lipoproteins (VLDL) and low density lipoproteins (LDL), and a fatty liver which contains cholesterol ester as its major lipid. The fatty liver secretes apoE into a recirculating perfusate at a significantly higher rate and produces cholesterol ester-rich, apoC-deficient VLDL with slower electrophoretic mobility than the triacylglycerol-rich VLDL produced by perfused normal livers. LDL, secreted in significant quantities by the perfused fatty liver, but not by the normal liver, is also cholesterol rich and contains apoE as well as apoB. The incorporation of [(3)H]leucine into apoVLDL and apoLDL secreted by the livers of the hypercholesterolemic animals and the apoVLDL secreted by the normal liver corresponds to the pattern visualized when the apoproteins are separated by polyacrylamide gel electrophoresis. Similar patterns are noted when non-recirculating perfusates are studied. These results indicate that the cholesterol ester-rich, apoC-deficient VLDL and the apoE-containing LDL found in the serum of hypercholesterolemic rats are not solely catabolic remnants of VLDL and chylomicrons but are secreted by the liver. Separation of the perfusate lipoproteins by agarose gel filtration revealed that most of the apoE secreted by the livers of hypercholesterolemic rats is found in the VLDL and LDL, whereas apoE secreted by the normal livers is distributed equally between VLDL, high density lipoproteins, and a low molecular weight fraction which corresponds to the virtually delipidated apoprotein. Thus the distribution of apoE among the lipoprotein fractions may be related to the total amount of cholesterol being transported in the circulation.
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PMID:Secretion of cholesterol-rich lipoproteins by perfused livers of hypercholesterolemic rats. 22 14

Liver function tests were performed in severe and mild diabetic rats and under the influence of ATP. In mild diabetics the serum cholesterol was significantly increased, while in severe diabetes the serum cholesterol was significantly lower than in mild diabetes. The decreased serum cholesterol in severe diabetes may be an indication for the development of fatty liver. The serum alkaline phosphatase and serum bilirubin were significantly increased in both the severe and mild diabetic states, while the thymol turbidity test was insignificantly changed in both states of diabetes. Serum albumin was significantly decreased in 10 days mild diabetes, while it was insignificantly changed in 48 hrs severe diabetic animals. The effect of ATP was investigated in mild diabetes. ATP resulted in a significant increase in serum albumin and a decrease in total globulins with the resultant increase in A/G ratio. The serum alkaline phosphatase exhibited a significant reduction under the influence of ATP. The elevated cholesterol of mild diabetic rats remained significantly elevated and was not reduced by ATP, though the fat content of the liver showed a significant reduction. This may be due to more rapid mobilisation of fat from the liver under the influence of ATP. ATP showed no significant effect on serum bilirubin and thymol turbidity test. the histopathological examination of the liver revealed that administration of ATP to alloxan diabetic rats had a beneficial effect. It resulted in disappearrance of the fat globules from the liver cells.
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PMID:Effect of ATP on liver function tests in experimental diabetes. 65 50

Adult male mice were made hypercholesterolemic by a diet high in cholesterol, cholic acid, animal fat, and sucrose. After three months on this diet, animals were infected with 5 X 10(9) plaque-forming units of coxsackievirus B5. Control groups consisted of uninfected hypercholesterolemic mice and infected mice maintained on a standard laboratory diet. Infection in the hypercholesterolemic animals was associated with leukopenia, severe fatty metamorphosis and focal necrosis in the liver, cholelithiasis, ileus, cardiomyolysis, and lack of inflammatory response. These mice died within seven to 14 days. Uninfected hypercholesterolemic animals had lesser degrees of fatty liver and cholelithiasis, and all survived. Infected mice maintained on a standard diet also survived. Titers of virus in representative tissues were lower in the hypercholesterolemic than in the normal mice, an indication that replication of virus was not solely responsible for the lethal outcome of the infections. These experiments demonstrate that hypercholesterolemia may alter host defenses against group B coxsackievirus in the mouse.
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PMID:Infection of hypercholesterolemic mice with Coxsackievirus B. 93 93

A high cholesterol/cholate diet induced hypercholesterolemia and fatty liver in both spontaneously hypertensive rats (SHR) and normotensive control rats (WKY). However, in contrast to previous concepts, the levels of cholesterol ester, triacylglycerol and phosphatidylcholine in plasma as well as triacylglycerol in liver were higher in WKY than in SHR fed a normal diet. The high cholesterol/cholate diet elevated the levels of plasma cholesterol, plasma cholesterol ester and hepatic triacylglycerol, and the extent of elevation was significantly higher in WKY than in SHR. Increases both in monoene/saturated ratios, an indication of elevated delta 9-desaturase activity, and in linoleate/arachidonate ratios, a possible indication of impaired desaturation-elongation activity, were observed in hepatic and plasma lipids of both strains fed the high cholesterol/cholate diet. The increases in monoene/saturated ratios were similar in both strains, but the increases in the linoleate/arachidonate ratios were higher for the plasma cholesterol esters of WKY than of SHR. The n-6/n-3 ratios of plasma and hepatic lipids were higher in WKY than in SHR throughout the experiments. These diet-induced changes observed in hepatic and plasma lipids were not reflected in the aortic lipids. Thus, hypertension per se does not promote the development of hyperlipemia and fatty liver induced by a high cholesterol/cholate diet. Our results also suggest that the metabolism of polyenoic fatty acids is different between SHR and WKY.
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PMID:Hypertension does not stimulate the development of hypercholesterolemia or fatty liver induced by a high cholesterol/cholate diet in rats. 280 64

A pilot study to improve unhealthy life habits of thirty middle-aged male clerical workers (45 +/- 3.58 yr.) with mild health disorders such as hypertension, hypercholesterolemia, diabetes mellitus and fatty liver was carried out. Under prohibition of smoking and alcohol intake, they spent five nights and six days at a hot spring resort, taking part in planned health training programs which included aerobic training, hiking in forests, hot spring baths, cooking practice and lectures about healthy life, controlled by medical, dietary and physical training staffs. To evaluate the short-term effects of these activities, body weight, blood pressure, serum lipid (total cholesterol, high-density-lipoprotein cholesterol, triglyceride, total free fatty acid and phospholipid), blood sugar, uric acid, gamma-glutamyl transpeptidase (gamma-GTP) and glutamic-oxaloacetic transaminase (GOT) were examined early in the morning of the second (before) and the fifth (after) days, and then their impressions of these recreation activities were monitored by questionnaires on the sixth day. By t-tests of all before-and-after data, it was shown that mean values of body weight, systolic blood pressure, high-density-lipoprotein cholesterol, triglyceride, phospholipid and gamma-GTP were improved, but fasting blood sugar, uric acid and GOT were not improved. In comparison of blood pressure levels, the hypertensive group (n = 9) showed lowering in both systolic and diastolic blood pressure, though the normal group (n = 10) had slight elevation. In addition, in the hypercholesterolemic group (n = 11, greater than or equal to 220 mg/dl) mean total cholesterol values decreased, conversely in the hypocholesterolemic group (n = 6, less than 180 mg/dl) they increased. Moreover, the obese group (n = 15, obesity index greater than or equal to 120%) showed greater decreases of body weight, triglyceride and phospholipid than the non-obese group. From questionnaires, it was confirmed that through these recreation activities most participants found mental and spiritual satisfaction, in spite of heavy physical loads. The short-term recreation activities under a stressless environment seemed to maintain the function of homeostasis in the body, but further investigation is needed to examine the relation between the contents of diets and physical activities, and to follow the long-term effects on the participants.
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PMID:[A study on the physical effects of short-time recreation activities at a hot spring resort on unhealthy middle-aged workers]. 281 Aug 61

1000 consecutive blood donors had their liver functions studied. 110 donors (11%) were found to have raised ALT of more than twice normal levels. 29 donors had liver biopsies done. Histologically 23 had fatty change, 5 had chronic persistent hepatitis and 1 had liver cirrhosis. Fourteen out of the 23 donors with fatty change also had hypercholesterolemia and hypertriglyceridemia. Viral serology of the 110 donors showed that 3 donors were HBsAg positive, 5 donors were Anti-HAV (IgM) positive and 20 donors were Anti-HBc (IgM) positive. Majority of donors with raised ALT had fatty liver on biopsy with only 6 donors having significant findings of chronic persistent hepatitis and cirrhosis. Serologically, most of the donors (74.5%) with raised ALT had no markers of Hepatitis A, Hepatitis B, CMV or EBV. An interesting finding is the high incidence (18%) of positive, Anti HBc (IgM) in donors with raised ALT.
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PMID:Liver disease in blood donors with raised transaminases. 375 95

Lipid peroxidation has been induced by means of an atherogenic diet causing hypercholesterolaemia, hypertriglyceridaemia, increased LDL and decreased HDL serum fractions in addition to the fatty degeneration, vacuolization of the liver cells and accumulation of malondialdehyde in the liver. Increased release of acid phosphatase and N-beta-glucuronidase was also observed pointing to cholesterol-induced lysosomal membrane damage. In response to pretreatment with, and simultaneous administration of, 6,6'-methylene bis (2,2-dimethyl-4-methane sulphonic acid sodium salt-1,2-dihydroquinoline) the signs and symptoms of fatty liver degeneration, the tissue, plasma and platelet malondialdehyde concentrations and the LDL serum fraction significantly decreased and HDL serum fraction increased. Lisosomal membrane stability was restored, resulting in physiological acid phosphatase and N-beta-glucuronidase activities. The pathological and clinical aspects of lipid peroxidation in several diseases of the digestive organs and the suggested therapeutic uses of non-toxic radical scavengers have been outlined.
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PMID:Liver lipid peroxidation induced by cholesterol and its treatment with a dihydroquinoline type free radical scavenger in rabbits. 653 29

Ten laying hens with low plasma cholesterol levels and no signs of fatty liver syndrome were examined at necropsy. Liver coloration and deposition of body fat were not abnormal in such hens. Eleven nonlaying hens had signs of fatty liver syndrome. They were out of production for 1 to 3 months and had elevate plasma cholesterol levels. At necropsy, such hens had yellow livers, heavy deposits of body fat, and several involuted egg yolks, which were dark yellow. Intimal plaques were observed by light microscopy in the abdominal aortas of hens with low plasma cholesterol levels; the plaques contained little or no lipid and were composed of three or four rows of modified smooth-muscle cells. Aortic intimal plaques of hens with high plasma cholesterol levels were composed of 16 to 18 rows of modified smooth-muscle cells when examined by light microscopy. The plaques contained intracellular and extracellular lipid, indicating aortic atherosclerosis. Electron-microscopic observations of the abdominal aortas of both groups of hens were similar to light-microscopic observations, except that lipid, including cholesterol clefts, was seen both intracellularly and extracellularly in the thickened tunica intima of hens with high plasma cholesterol values. Thus, the presence of aortic atherosclerosis was confirmed by electron microscopy. It is suggested that the endogenous hypercholesterolemia and cessation of egg production, characteristic of severe fatty liver syndrome, originated from the reabsorption of involuted egg yolks and that such reabsorption caused the development of aortic atherosclerosis and deposition of excess body fat.
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PMID:Aortic atherosclerosis in nonlaying hens with fatty liver syndrome. 663 49

Using fractionation, subcellular pathogenesis of the fatty liver was investigated. Floating lipids were isolated from a small amount of the liver obtained by needle biopsy. The volume of the floating lipids was correlated to the grading of fat infiltration of the intact tissue. Of lipid-rich particles bound by membranous structures, the volume of lipolysosomes in the patients with liver damage associated with diabetes mellitus was greater than that of alcoholics. Hypercholesterolemia was another feature characteristic of the liver disease exhibiting lipolysosome proliferation. These observations suggest a lysosomal involvement in fatty degeneration of the liver in diabetics through an overload of cholesterol.
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PMID:Electron microscopic study on the floating lipids of human liver. Lysosomal involvement in the fatty liver associated with diabetes mellitus. 665 Jan 72


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