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Results for “LIVER CIRRHOSIS, EXPERIMENTAL”

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PubMed2000

The influence of dietary nucleotides and long-chain polyunsaturated fatty acids on the incorporation of [3H] arachidonic acid on experimental liver cirrhosis.

The purposes of this study were to determine: a) the incorporation of labeled [3H] arachidonic acid on the intestinal mucosa, the liver and plasma, after 1,3 and 5 hours of administration, b) preferential incorporation by different tissues, c) and the effects on experimental rats with thioacetamide-induced cirrhosis, after four weeks of a dietary supplementation with nucleotides and long-chain polyunsaturated fatty acids. 209 female Wistar rats were divided into two groups (control and TAA group). The TAA group was given 300 mg of thioacetamide/L, in their drinking water for four months. After this period, a sample of 6 rats were taken from each group and examined, to evaluate the biochemical and histological changes of the experimental model, and 36 rats were taken to determine the incorporation of radioactivity by the groups. The rest of the animals were divided into four subgroups. Each group, receiving a supplementary diet with only long-chain polyunsaturated fatty acids and/or nucleotides or neither, for 4 weeks. After four months of thioacetamide, the incorporation of the [3H] arachidonic acid showed: a) an increased within 3 h in the intestinal mucosa, b) a decreased in the liver after 3 to 5 h c) and a drastic decrease in the plasma after 3 to 5 h. With a dietary supplementation of long-chain polyunsaturated fatty acids and nucleotides combined, there was a decrease of accumulate [3H] arachidonic acid in the intestine and a increase in the liver and plasma. The simultaneous supply of dietary polyunsaturated fatty acids and nucleotides was beneficial in the reversal of abnormalities of the lipid metabolism, in this experimental model of liver cirrhosis.

Analysis of Variance↗
PubMedDate not supplied

Insulin-degrading activity in experimental liver cirrhosis of the rat.

Liver cirrhosis in man is often associated with hyperinsulinemia but its pathogenesis is still unexplained. To investigate whether insulin degradation is impaired in cirrhotic liver, the specific insulin-degrading enzyme activity (EC 3.4.22.11) was assayed in liver cytosol of rats with CCl4-induced liver cirrhosis. No difference was found between liver cytosol of cirrhotic and control rats. The results show that experimental CCl4-induced liver cirrhosis does not damage the specific insulin-degrading activity and support the hypothesis that impaired hepatic insulin handling is not an important cause of hyperinsulinemia in liver cirrhosis.

Animals↗
PubMed1989

Glutathione synthesis and export in experimental liver cirrhosis induced by thioacetamide: relations to ultrastructural changes.

Micro-and macronodular experimental liver cirrhosis was induced in female rats by administration of 0.03% thioacetamide (TAA) in drinking water for 3 or 6 months, respectively. The glutathione (GSH) status (content, synthesis, export) and ultrastructural changes of liver were investigated 14 d after withdrawal of TAA. The hepatic level of GSH was increased after 6 months TAA treatment. The levels of oxidized glutathione (GSSG) were not changed after 3 months or 6 months TAA administration. The GSH synthesis was not disturbed in the cirrhotic livers; only the ratio between the 2 synthesizing enzymes was changed in macronodular liver cirrhosis. The plasma GSH content was reduced in both cases, independent of the stage of liver cirrhosis. The electron microscopic studies on cirrhotic rat livers revealed a series of characteristic structural changes, such as disorganization and total lack of the microvilli border, appearance of basement membrane-like deposits within the narrowed space of Disse, disappearance of the highly porous endothelial cell lining and partly an intensively detoriated blood supply within the pseudolobules. It is suggested that all these changes may contribute to a disturbance of the GSH export from the hepatocytes into the blood. It is very likely, however, that the alterations of the sinusoidal cell surface play the most important role. 1. The GSH/GSSG redox potential is shifted in favour of the reduced form in this cirrhosis model. This shift seems to be connected with later stages of cirrhogenesis. 2. A GSH export disturbance is responsible for the decreased plasma GSH level in liver cirrhosis.

Animals↗
PubMed1991

Gamma-glutamyltranspeptidase (GGT) in experimental liver cirrhosis induced by thioacetamide: a biochemical and enzymehistochemical study.

Micro- and macronodular experimental cirrhosis-like liver lesion was induced in female rats by administration of 0.03% thioacetamide (TAA) in drinking water for 3 or 6 months. The activity of gamma-glutamyltranspeptidase (GGT) and the distribution pattern of this enzyme within the liver structure were investigated 14 d after withdrawal of TAA in comparison to neonatal and adult normal liver. GGT activity was extremely high at birth. Chronic TAA administration led to a strong increase in hepatic GGT activity in dependence on duration of TAA administration in comparison to adult controls. In accordance to these results we observed by enzyme-histochemistry a small to moderate hepatocellular GGT activity after 3 months of TAA treatment. GGT activity was also demonstrable in epithelia of proliferated ductuli biliferi of single enlarged portal tracts. After 6 months of TAA administration the hepatocellular GGT activity was moderate to strong. It was demonstrable both in parenchymal (preneo-plastic) nodules and in cholangiocellular/cholangioductular proliferates. A GGT activity of mesenchymal cells was not demonstrable. We conclude that the increased hepatic GGT activity after chronic TAA administration can be correlated with the process of development of preneoplastic nodules. A relation between increased GGT activity and the process of cirrhogenesis does not seem to be probable in this animal cirrhosis model.

Animals↗
PubMed2000

Elevated serum dipeptidyl peptidase IV (CD26, EC 3.4.14.5) activity in experimental liver cirrhosis.

BACKGROUND: Dipeptidyl peptidase IV (DPP IV) is a cell surface ectoenzyme widely distributed in the rat body, present on the epithelial cells of the brush border membranes (e.g. bile canaliculi) and on the surface of reactive lymphocytes and fibroblasts. DPP IV has been implicated in hepatocyte-extracellular matrix interactions, fibroblast activation and proliferation and in T-cell activation. Aberrant DPP IV expression was found in human liver cirrhosis, and elevated serum DPP IV activity was reported in patients with primary biliary cirrhosis and chronic hepatitis C virus infection. The aim of the study was to examine serum DPP IV activity in experimental liver cirrhosis. METHODS: Liver cirrhosis was induced by administering diethyl-nitrosamine, phenobarbital and CCl4 in Fischer-344 male rats (n = 22). Phenobarbital-treated (n = 9) and nontreated (n = 9) male rats were used as controls. Serum DPP IV activity was measured using a microplate-based continuous-monitoring assay. Recombinant rat DPP IV was used as standard and Gly-Pro-PNA was used as substrate. Enzyme activity was given in nmol mL-1 min-1 (U L-1). RESULTS: Significantly higher DPP IV activity was found in the sera of rats with experimental liver cirrhosis (39.2 +/- 3.7; mean +/- SD) compared to phenobarbital-treated (11 +/- 4, P < 0.000002) and nontreated (10.9 +/- 0.9, P < 0.000002) rats. There was a positive correlation between DPP IV activity and concentrations of aspartate aminotransferase (r = 0.73, P = 0.0001) and alanine aminotransferase (r = 0.69, P = 0.0004). CONCLUSIONS: The significantly higher serum DPP IV activity found in experimental liver cirrhosis is in concordance with human observations. The elevation was probably not due to the enzyme induction effect of phenobarbital. In this experimental model, serum DPP IV seems to be an indicator for chronic liver injury.

Animals↗
PubMed1982

[State of the air-blood barrier in experimental liver cirrhosis].

Changes in the structure of the aerohematic barrier of the lungs were found in experimental liver cirrhosis in mice produced by administration of CCl4. The barrier was markedly thicker due to increased amounts of collagen microfibrils and elastic structures, there were degenerative changes of pneumocytes of the I and II type, as well as of endotheliocytes.

Animals↗