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

Collagenisation of the space of Disse was systematically assessed to determine its relationship to the clinical and histological manifestations of chronic alcoholic liver disease. Ninety-four chronic alcoholics who had been submitted to biopsy were assessed by clinical manifestations of hepatic dysfunction and by a 17-parameter Combined Clinical and Laboratory Index (CCLI). Liver biopsies were scored for light (LM) and electron-microscopy (EM) abnormalities using a universal scoring system for both. Thirty-five patients with normal liver histology (LM) had an average collagen score of 0.6 +/- 0.1. Twelve cirrhotic patients and 29 with fatty liver, both groups with mild clinical manifestations, did not differ significantly. In 18 cirrhotic patients and five with fatty liver, both groups having severe clinical manifestations, the mean scores were 2.1 +/- 0.8 (P less than 0.02) and 2.5 +/- 0.6 (P less than 0.01) respectively. Collagenisation also correlated with CCLI (P less than 0.001), serum bilirubin (P less than 0.001), serum aspartate transferase (SGOT) (P less than 0.003), and clinical evidence of portal hypertension and histological changes of necrosis, inflammation, and terminal hepatic vein sclerosis. These results suggest that collagenisation of the Disse space may be important in the pathogenesis of alcoholic liver disease.
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PMID:Collagenisation of the Disse space in alcoholic liver disease. 48 62

Changes of alkaline phosphatase activity in the process of healing liver injuries of rats on which partial hepatectomy was performed were the subject of our researches. Reaction on alkaline phosphatase was performed on cryostat sections according to the method of Gomori-Takamatsu. It has been found that granulated precipitate of cobalt sulphide was localized in the cytoplasm of granulocytes, macrophages and fibroblasts. A diffusive reaction comprized clusters of newly created collagen fibres. In early stages in the centres of necrosis, the activity of alkaline phosphatase increased, in later periods a lack of the activity was observed. Steatosis of liver tissue does not correlate with the intensity of the reaction. Lack of alkaline phosphatase activity is characteristic for old cicatrices. The authors discuss the effects of the histogenetical process during healing of liver injury on the results of the histoenzymatic reactions. The authors suggest that alkaline phosphatase is involved in the mechanism of re-building collagen fibres. It is stressed in the conclusion that the localization and intensity of alkaline phosphatase in the area of healing liver lesions are variable depending on the period of healing wound of the liver and the influence of other complications.
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PMID:Activity of alkaline phosphatase in the healing rat liver after hepatectomy. 74 40

Rats were fed a high cholesterol, olive oil diet for one or seven weeks. The resulting hypertrophic fatty livers were analyzed for lipids, nucleic acids, and connective tissue components. The cholesterol and neutral glyceride contents of liver increased approximately 30-fold during the first week while phospholipids remained almost unchanged. After seven weeks the accumulation of cholesterol was further increased and the content of phospholipids enhanced. The total amounts of DNA and RNA rose with increasing weight of fatty liver. In seven weeks the diet caused a marked increase in hepatic collagen and glycosaminoglycans. The synthesis of collagen was increased in fatty liver slices after both one and seven weeks of the experiment. Fatty liver produced by this lipid diet is suggested as a suitable model for studying the mechanism by which lipids stimulate hepatic fibroblasts.
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PMID:Effect of high cholesterol, olive oil diet on the lipids and connective tissue in rat liver. A biochemical study. 100 61

Percutaneous liver biopsies obtained from patients with a history of chronic alcoholism and normal liver, fatty liver, alcoholic hepatitis, or active cirrhosis were incubated with tritiated proline to determine the pattern of collagen biosynthesis in these conditions. Incorporation of labeled proline and hydroxyproline into salt-soluble and insoluble fractions of collagen was evaluated by radiochemical analysis and tissue localization documented by autoradiography. Biopsy specimens of alcoholic hepatitis and cirrhosis exhibit a significant increase in the amount of radioactive proline and hydroxyproline in salt-soluble and insoluble collagen. Marked accumulation of radioactivity occurred over bile ducts, fibroblasts, and collagen fibers in the portal area and over hepatocytes, fibroblasts, and collagen fibers in the centrilobular area. Fatty liver is associated with an increase in uptake of proline and hydroxyproline in the salt-soluble fraction of collagem; silver grains appear in the periphery of fat-laden cells and in areas of focal inflammation. Digestion by collagenase indicates that labeling over fibroblasts and collagen reflects active synthesis, whereas, entry of proline into the cell protein pool is responsible for accumulation of radioactivity in other sites. In vitro ethanol causes a significant increase in the incorporation of proline and hydroxyproline into collagen in biopsy specimens of alcoholic hepatitis or active cirrhosis, but has no effect on collagen synthesis by normal or fatty liver.
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PMID:Collagen biosynthesis in liver disease of the alcoholic. 117 Feb 67

Previous studies have shown that alpha-tocopherol (vitamin E) pretreatment of experimental animals can protect against acute liver necrosis induced by carbon tetrachloride. In this study we investigated whether the increase of vitamin E liver content by dietary supplementation influences chronic liver damage and cirrhosis induced by carbon tetrachloride in the rat. Our data indicate that vitamin E supplementation did not interfere with the growth rate of the animals and increased about threefold the liver's content of the vitamin. Vitamin E supplementation significantly reduced oxidative liver damage, but it was not effective in protecting against development of fatty liver and did not interfere with metabolic activation of carbon tetrachloride. Moreover, vitamin E-fed animals showed incomplete but significant prevention of liver necrosis and cirrhosis induced by carbon tetrachloride. This has been shown by means of histological examination, analysis of serum parameters and biochemical evaluation of collagen content. These results show that an increased liver content of vitamin E can afford a significant degree of protection against carbon tetrachloride-induced chronic liver damage and cirrhosis.
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PMID:Vitamin E dietary supplementation protects against carbon tetrachloride-induced chronic liver damage and cirrhosis. 139 81

Four markers for hepatic fibrosis--N-terminal peptide of Type III procollagen (PIIIP), Laminin P1 (laminin), Type IV collagen (Type IV-C), and 7S domain (7S)--were measured in the sera of 90 patients with various chronic liver diseases diagnosed by liver biopsy--fatty liver (FL), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), and liver cirrhosis (LC)--and in the sera of 20 healthy controls. The values of markers were compared with the grade of histologic findings of the liver. Four markers were significantly raised in the CAH group and the LC group, and they were considered to be indicators of hepatic fibrosis. PIIIP reflected necrosis and inflammation as well as fibrosis of the liver. Laminin, Type IV-C, and 7S reflected severe fibrosis. 7S was considered to be useful marker for liver cirrhosis.
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PMID:[Clinical significance of measurement of PIIIP, laminin P1, type IV-C and 7S in patients with chronic liver diseases--with special reference to histological findings]. 140 88

Histopathological changes in alcoholic liver disease are characterized by Mallory body, fatty liver, and peculiar fibrosis such as pericentral fibrosis, pericellular fibrosis, stellate fibrosis originating from Glisson's sheath, and swelling of the liver cells. However, the mechanism of fibrosis remains unknown. The author tried to demonstrate, by the immunohistochemical method, fibronectin (FN), collagen type I, III, IV (IC, IIIC, IVC), factor XIIIa, and factor VIII related antigen (VIII RAg), all of which are related to the process of wound healing, in order to clarify the mechanism of fibrosis in alcoholic liver disease. With the progress of fibrosis, FN was demonstrated in the sinusoidal wall, as well as the portal areas and around the central veins. IC and IIIC were positive in the fibrotic area extending into the lobules and pericellular fibrosis. IVC was similar to FN and was positive in the sinusoidal wall. Scattered XIIIa positivity was recognized in the fibrotic areas, especially in the foci of active fibrosis. VIII RAg was positive in the capillary vessels invading the lobules through the limiting plates. The distribution of these proteins in the fibrotic area in alcoholic liver disease closely resembled that in the wound healing process. It is concluded that fibrosis occurring in the periportal area is essentially the same as in the wound healing process and the mechanism of fibrosis in alcoholic liver disease is thought to be active fibroplasia.
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PMID:[Immunohistochemical study of the distribution of collagens (type I, III, IV), fibronectin, factor XIIIa and factor VIII related antigen in alcoholic liver disease]. 168 Aug 76

Bronfenmajer et al. (1966) first studied Ito cells in alcoholic hepatitis (AH) by light microscopy (LM). The number of Ito cells and the number of fat droplets were increased. Okanoue et al. (1983) found that Ito cells were reduced by LM but increased by electron microscopy (EM) in scars in AH. Ito cells were activated in scars (increased RER and decreased fat in Ito cells with transition to fibroblasts). Minato et al. (1983) showed that increased RER in Ito cells correlated with increased collagen synthesis of liver biopsies in vitro. Mak et al. showed increased RER correlated with the degree of fibrosis in alcoholic baboons (1984) and alcoholic cirrhosis in man (1988). French et al. (1988b) showed morphometrically that Ito cell fat was decreased and RER was increased only in scars but not in normal sinusoids so that Ito cell activation was restricted to the scars. There was no correlation of sinusoidally located Ito cell fat or RER with the amount of perisinusoidal collagen. In rats fed ethanol and a nutritionally adequate diet including corn oil (25% of calories) by intragastric cannula for five months the fatty liver progressed to focal central fibrosis, and Ito cell activation (fat/RER) was increased. When tallow was substituted for corn oil the Ito cells were not activated and the liver histology was normal. Thus, the type of dietary fat and the local environment (scars) are important factors in the activation of Ito cells by alcohol in vivo.
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PMID:Ito cell activation induced by chronic ethanol feeding in the presence of different dietary fats. 184 63

The authors examined the aminoterminal type III procollagen peptide level of serums and killer-cell activity peripheric blood lymphocytes with 75 patients suffering from ethanol originated liver diseases as well as control samples from 40 healthy volunteers. Determination of type III procollagen peptide (Fab) took place by the RIA method. The cytotoxic activity of killer-cells was tested against human red blood cells. Both in fatty liver and chronic alcoholic hepatitis the level of type III procollagen peptide increased, while in liver cirrhosis the same level reached a value three times of the normal. At the same time in cirrhosis hepatitis an increased killer-cell activity could be observed. Type III procollagen peptide values were also analysed in view of the cytotoxic capacity of killer-cells. At first ill, then healthy control individuals were divided into three groups according killer-cell activity values. Results have shown that in the group with a high level killer-cell activity average type III procollagen peptide values were significantly greater as compared to those of the medium or low level activity groups. These results might indicate a relation between a conditional antibody-dependent cellular cytotoxicity reaction and increasing collagen synthesis.
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PMID:[Serum aminoterminal type III procollagen peptide level and killer cell activity in patients with alcoholic liver diseases]. 195 78

The experimental hepatic lesion of C57 mice was induced by carbon tetrachloride (CCI4), and the feeds containing pollen of Codonopsis pilosula were given to the animals. It was found by electronic microscopy that these pollens evidently reduced the hepatic steatosis, improved liver necrosis, suppressed the formation of the collagen fibrils in Disse's spaces and around central veinules. It was shown that the pollens of Codonopsis pilosula could counteract efficiently the liver lesion of mice induced by CCI4.
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PMID:[Protective effects of the pollen of Codonopsis pilosula (Franch.) Nannf. on liver lesions at the ultrastructural level]. 250 6


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