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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 dietary sucrose concentrations in the development of hepatic steatosis in rats was investigated. Twelve groups of weanling male Sprague-Dawley rats received semipurified diets with different sucrose concentrations ranging from 20 to 50% (w/w); one group received a cereal-based chow diet. Rats were sacrificed after 3 weeks and body weight, liver/body weight ratio, plasma alanine aminotransferase concentration, hepatic triglyceride concentration, and liver morphology (light and electron microscopy) were determined. Body weight and liver/body weight ratio were decreased in rats receiving 40-50 or 25-35% dietary sucrose compared to rats receiving 20% sucrose or chow. Plasma alanine aminotransferase concentrations were within normal limits. Hepatic triglyceride concentration was significantly increased in rats receiving 40-50 and 25-35% dietary sucrose compared to rats receiving 20% dietary sucrose or chow. Light microscopy showed hepatic steatosis in a periportal distribution at all concentrations of dietary sucrose. Both the frequency and the severity of the steatosis were increased with increasing dietary sucrose concentrations. Electron microscopy from selected livers with increased hepatic triglyceride concentrations revealed increased lipid spheres and increased smooth endoplasmic reticulum without prominent Golgi apparatus or GERL complex. It is concluded that high dietary sucrose concentrations are responsible for the development of hepatic steatosis. Semipurified diets with high dietary sucrose concentrations such as the AIN-76A diet (50% sucrose) should not be used in animal studies in which increased triglyceride deposition could influence experimental outcome.
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PMID:Hepatic steatosis in rats fed diets with varying concentrations of sucrose. 651 Jun 14

Fatty liver was induced in the rats shortly after administration of cycloheximide, ethionine, orotic acid, monensin or colchicine. It was strongly suggested that derangements in one or more of the hepatic lipoprotein metabolic steps, which occur at the levels of endoplasmic reticulum, Golgi apparatus and secretory vacuoles lead to an accumulation of triglyceride within hepatocytes.
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PMID:Ultrastructural changes of hepatocyte organelles induced by chemicals and their relation to fat accumulation in the liver. 665 Jan 71

Fatty liver induced in rats by a high protein diet without pyridoxine was studied morphologically. The microscopic change was characterized by accumulation of fat in hepatocytes of the centrolobular and midzonal areas. Electron microscopic examination at an early stage showed marked accumulation of small osmiophilic particles in the granular endoplasmic reticulum and vesicles throughout the cytoplasm with similar particles in the spaces of Disse. After 4 weeks, numerous lipid droplets of various sizes were seen in pericanalicular lysosomes in hepatocytes with concomitant increase in the triglyceride level. The droplets gradually formed larger droplets in the cytoplasm. After 8 weeks, myelin figures together with fat droplets were seen in continuity with the endoplasmic reticulum and occasionally crystal clefts were observed within lysosomes of hepatocytes. These findings suggest that development of fatty liver results from impaired lysosomal degradation of lipid.
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PMID:Pathogenesis of fatty liver in rats fed a high protein diet without pyridoxine. 705 68

The contribution of subcellular organelles in egg yolk-induced fatty liver was investigated in liver tissue sections and fractionated liver homogenates. When 2.0 ml. of 12.5 per cent egg yolk were administered to Wistar male rats (body weight, 250 to 350 gm.), a fatty change occurred in the liver after a 4-hour period. The acute fatty liver was characterized by intralysosomal accumulations of fat. The number of fat-containing lysosomes increased as early as 30 minutes after egg yolk administration. During this period, fat infiltration was not evident elsewhere in the cytoplasm. The increase of these lysosomes in tissue sections coincided with a selective proliferation of lipolysosomes in the heavy subfraction of floating lipids of liver homogenate. Neither Golgi-derived dense bodies of very low density lipoproteins nor vesicles of the endoplasmic reticulum increased in number throughout the experimental period. These observations indicate that hepatic lysosomes are involved in the degradation of exogenous cholesterol and that transformation of lysosomes to lipolysosomes is a direct result of cholesterol overload and not simply a manifestation of fatty liver.
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PMID:Egg yolk-induced lipolysosome proliferation and fat infiltration of rat liver. 720 81

A 35-year-old man, sephardic jew, complains for the last eleven years of typical and frequent attacks of FMF. His liver is hypertrophic. Needle-biopsy reveals an extensive macrovacuolar triglyceride storage (60 per cent) and an active vascular congestion with erythrodiapedesis in the mild and centrolobular zone, without any necrosis, cellular infiltration nor fibrosis. Electron microscopy shows lipofuschin deposits and mild lesions of mitochondrias, endoplasmic reticulum. Blood triglycerides and apo B are rather low. After six weeks of colchicine treatment, needle biopsy shows no more active congestion nor erythrodiapedesis. Triglyceride storage lowers to 40 per cent. After seven months of colchicine treatment, triglyceride storage falls down to 12 per cent. FMF may be considered as a cause of fatty liver when there is not any cause else and only after deep decrease or disparition of triglyceride deposit by a long time colchicine treatment.
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PMID:[Familial Mediterranean fever and fatty liver. effect of a long time colchicine treatment on triglyceride storage (author's transl)]. 733 25

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

The pathology of post-parturient fatty liver has been studied in a group of 20 high-yielding dairy cows; 10 had less than 20 per cent fat in the liver cell and were classified as having a mild fatty liver and 10 had more than 30 per cent fat in the liver cell and were classified as having severe fatty liver. Severe fatty liver was accompanied by a number of morphological changes including the occurrence of lipogranulomas, increased liver cell volume, decreased volume of rough endoplasmic reticulum per liver cell and evidence of mitochondrial damage. The latter two changes were reflected in reduced albumin levels and increased activities of mitochondrial enzymes observed in the blood of cows with severe fatty liver. Reduced fertility may be one of the consequences of severe fatty liver in the dairy cow.
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PMID:The pathology of post-parturient fatty liver in high-yielding dairy cows. 742 83

The effects of carbon tetrachloride (CCl4) on the liver in spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) were investigated ultrastructurally in this study. Repetition of CCl4 treatment twice a week for four weeks, revealed liver cirrhosis in SHR, whereas, only bridging fibrosis was observed in the WKY, histologically, by reticulin silver impregnation. Scanning electron microscopy revealed that the liver surface of SHR was irregularly nodulated, while it was relatively smooth in case of the WKY. Transmission electron microscopy revealed that the mitochondria cristae were peripherally located in both strains. Vesicular change of the rough endoplasmic reticulum was observed to be more severe in SHR than in WKY. Further, local hypertrophy of the smooth endoplasmic reticulum and large lipid droplets were more easily observed in WKY than in SHR. The present results hence indicate that chronic chemical CCl4 intoxication induces severe ultrastructural organelle damage in hypertensive rats, leading to liver cirrhosis. On the other hand, CCl4 induced fatty liver and a relatively mild fibrosis were observed in normotensive rats. These findings suggest that the liver ultrastructural organelles are more susceptible to CCl4 in SHR than in WKY.
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PMID:Ultrastructural changes in liver damage induced by carbon tetrachloride in spontaneously hypertensive rats and Wistar-Kyoto rats. 968 7

A deficiency in microsomal triglyceride transfer protein (MTP) causes the human lipoprotein deficiency syndrome abetalipoproteinemia. However, the role of MTP in the assembly and secretion of VLDL in the liver is not precisely understood. It is not clear, for instance, whether MTP is required to move the bulk of triglycerides into the lumen of the endoplasmic reticulum (ER) during the assembly of VLDL particles. To define MTP's role in hepatic lipoprotein assembly, we recently knocked out the mouse MTP gene (Mttp). Unfortunately, achieving our objective was thwarted by a lethal embryonic phenotype. In this study, we produced mice harboring a "floxed" Mttp allele and then used Cre-mediated recombination to generate liver-specific Mttp knockout mice. Inactivating the Mttp gene in the liver caused a striking reduction in VLDL triglycerides and large reductions in both VLDL/LDL and HDL cholesterol levels. The Mttp inactivation lowered apo B-100 levels in the plasma by >95% but reduced plasma apo B-48 levels by only approximately 20%. Histologic studies in liver-specific knockout mice revealed moderate hepatic steatosis. Ultrastructural studies of wild-type mouse livers revealed numerous VLDL-sized lipid-staining particles within membrane-bound compartments of the secretory pathway (ER and Golgi apparatus) and few cytosolic lipid droplets. In contrast, VLDL-sized lipid-staining particles were not observed in MTP-deficient hepatocytes, either in the ER or in the Golgi apparatus, and there were numerous cytosolic fat droplets. We conclude that MTP is essential for transferring the bulk of triglycerides into the lumen of the ER for VLDL assembly and is required for the secretion of apo B-100 from the liver.
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PMID:Analysis of the role of microsomal triglyceride transfer protein in the liver of tissue-specific knockout mice. 1022 72

Eighty-five male Han-Wistar rats were arranged into three groups: CCl4-exposed rats, CCl4 + betaine-exposed rats, and control rats. To see the effect of betaine alone, five rats of the control and of the CCl4 + betaine groups were sacrificed after 7 days, before exposure to CCl4. After that, two of the groups (the CCl4 and CCl4 + betaine groups) were exposed to CCl4 (1 ml/kg per day subcutaneously [SC] for 4 consecutive days), and one of the groups (control group) was given olive oil (1 ml/kg per day SC for 4 consecutive days). At the start of the study (day 0), day 1, day 2, day 3, day 4, and 3 days after the last CCl4 and olive oil injections (day 7), samples of five rats per group were sacrificed, and the livers were taken for chemical analyses and histological examination. Oral betaine, after the acclimation period of a week, increased the number of mitochondria but not mitochondria size (day 0), compared with the case in control rats. Exposure to CCl4 resulted in centrilobular hepatic steatosis, and the administration of betaine significantly reduced this. Morphometric analyses also revealed that the addition of betaine increased the volume density of rough endoplasmic reticulum (RER) in the perinuclear areas of liver cell cytoplasm (day 7). Additionally, the administration of betaine prevented the reduction of Golgi complexes and mitochondrial figures in the cytoplasm observed after the exposures to CCl4. Also, the volume density of mitochondria was smallest in the CCl4-group, but the difference was not statistically significant. The results indicate that oral betaine either improves recovery or reduces the toxic effects of CCl4 on cell organelles in liver cells of male Han-Wistar rats.
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PMID:Reduction of carbon tetrachloride-induced hepatotoxic effects by oral administration of betaine in male Han-Wistar rats: a morphometric histological study. 1081 Sep 87


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