glycogen has been researched along with Cholestasis* in 11 studies
1 review(s) available for glycogen and Cholestasis
Article | Year |
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Pathology of viral hepatitis.
Topics: Acute Disease; Biopsy; Cholestasis; Cytoplasm; Feces; Glycogen; Hepatitis A; Hepatitis B; Hepatitis B Antigens; Humans; Inclusion Bodies, Viral; Inflammation; Jaundice; Kupffer Cells; Liver; Lysosomes; Microscopy, Electron; Mitochondria, Liver; Necrosis; Ribosomes | 1972 |
10 other study(ies) available for glycogen and Cholestasis
Article | Year |
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Fasting reveals largely intact systemic lipid mobilization mechanisms in respiratory chain complex III deficient mice.
Mice homozygous for the human GRACILE syndrome mutation (Bcs1l Topics: Acidosis, Lactic; Animals; Blood Glucose; Cholestasis; Electron Transport; Electron Transport Complex III; Fasting; Female; Fetal Growth Retardation; Gluconeogenesis; Glycogen; Hemosiderosis; Hepatocytes; Homozygote; Hypoglycemia; Lipid Mobilization; Liver; Male; Metabolism, Inborn Errors; Mice; Mice, Inbred C57BL; Mitochondria; Mitochondrial Diseases; Renal Aminoacidurias; Triglycerides | 2020 |
Selection, proliferation and differentiation of bone marrow-derived liver stem cells with a culture system containing cholestatic serum in vitro.
To explore the feasibility of direct separation, selective proliferation and differentiation of the bone marrow-derived liver stem cells (BDLSC) from bone marrow cells with a culture system containing cholestatic serum in vitro.. Whole bone marrow cells of rats cultured in routine medium were replaced with conditioning selection media containing 20 mL/L, 50 mL/L, 70 mL/L, and 100 mL/L cholestatic sera, respectively, after they attached to the plates. The optimal concentration of cholestatic serum was determined according to the outcome of the selected cultures. Then the selected BDLSC were induced to proliferate and differentiate with the addition of hepatocyte growth factor (HGF). The morphology and phenotypic markers of BDLSC were characterized using immunohistochemistry, RT-PCR and electron microscopy. The metabolic functions of differentiated cells were also determined by glycogen staining and urea assay.. Bone marrow cells formed fibroblast-like but not hepatocyte-like colonies in the presence of 20 mL/L cholestatic serum. In 70 mL/L cholestatic serum, BDLSC colonies could be selected but could not maintain good growth status. In 100 mL/L cholestatic serum, all of the bone marrow cells were unable to survive. A 50 mL/L cholestatic serum was the optimal concentration for the selection of BDLSC at which BDLSC could survive while the other populations of the bone marrow cells could not. The selected BDLSC proliferated and differentiated after HGF was added. Hepatocyte-like colony-forming units (H-CFU) then were formed. H-CFU expressed markers of embryonic hepatocytes (AFP, albumin and cytokeratin 8/18), biliary cells (cytokeratin 19), hepatocyte functional proteins (transthyretin and cytochrome P450-2b1), and hepatocyte nuclear factors (HNF-1alpha and HNF-3beta). They also had glycogen storage and urea synthesis functions, two of the critical features of hepatocytes.. The selected medium containing cholestatic serum can select BDLSC from whole bone marrow cells. It will be a new way to provide a readily available alternate source of cells for clinical hepatocyte therapy. Topics: Animals; Blood Proteins; Cell Culture Techniques; Cell Differentiation; Cell Division; Cells, Cultured; Cholestasis; Common Bile Duct; Culture Media, Conditioned; Glycogen; Hematopoietic Stem Cells; Ligation; Liver; Phenotype; Rats; Rats, Sprague-Dawley | 2004 |
Rapid normalization of hepatic glycogen metabolism in rats with long-term bile duct ligation after biliodigestive anastomosis.
Rats with chronic bile duct ligation have reduced hepatic glycogen stores and decreased activities of enzyme involved in glycogen metabolism. In the current studies, the reversibility of these changes following reversal of biliary obstruction by Roux-en-Y anastomosis (RY) was investigated.. Rats were studied after bile duct ligation for 4 weeks (BDL rats), or 5 or 14 days after relief of biliary obstruction by RY. Control rats were pair-fed to treated rats, and all rats were studied in the fed state.. The liver glycogen content was decreased in BDL rats (198+/-167 vs. 753+/-315 mg/liver in BDL vs. control rats) and normalized within 5 days after RY. The total activities of glycogen synthase and phosphorylase were both reduced by 51% in BDL as compared to control rats. Five days after RY, the activity of glycogen synthase had increased significantly in comparison to BDL rats, whereas glycogen phosphorylase had remained unchanged. Fourteen days after RY, both enzyme activities had completely normalized. Northern blots revealed reduced hepatic mRNA levels in BDL rats, for glycogen synthase and phosphorylase. While the mRNA level for glycogen synthase normalized within 5 days after RY, the level for glycogen phosphorylase increased but did not normalize completely within 14 days after RY.. Hepatic glycogen stores are decreased in BDL rats but recover rapidly after relief of biliary obstruction. Reduced activity and mRNA levels of glycogen synthase suggest that impaired glycogen synthesis is the principal mechanism for decreased hepatic glycogen stores in BDL rats. Topics: Anastomosis, Roux-en-Y; Animals; Bile Ducts; Cholestasis; Glycogen; Glycogen Synthase; Ligation; Liver; Male; Phosphorylases; Rats; Rats, Sprague-Dawley; Reference Values; RNA, Messenger; Time Factors | 1999 |
Liver damage induced by acute cholestasis in the rat is ameliorated partially by L-arginine.
The aim of this paper was to determine if NO modulation would influence liver damage induced by 3 day-biliary obstruction. L-Arginine (500 mg kg-1, p.o. twice a day) or L-NAME (100 mg kg-1, p.o. twice a day) or both were administered to male Wistar rats subjected to bile duct ligation (BDL). In the liver, BDL doubled lipid peroxidation and depleted glycogen (P < 0.05), L-arginine completely prevented the former and partially the latter. Alkaline phosphatase, alanine aminotransferase and gamma-glutamyl transpeptidase serum enzyme activities increased (P < 0.05) by BDL, again L-arginine treatment partially, but significantly, prevented the elevation in these three markers of liver damage. Although L-NAME treatment failed to induce a change in any marker of liver injury studied herein, it abolished the beneficial effects of L-arginine, suggesting that these effects are probably mediated by NO synthesis stimulation. Topics: Alanine Transaminase; Alkaline Phosphatase; Animals; Arginine; Cholestasis; Enzyme Inhibitors; gamma-Glutamyltransferase; Glycogen; Lipid Peroxides; Liver; Male; NG-Nitroarginine Methyl Ester; Rats; Rats, Wistar | 1998 |
Morphology of the liver of the brook lamprey, Lampetra lamottenii before and during infection with the nematode, Truttaedacnitis stelmioides, hepatocytes, sinusoids, and perisinusoidal cells.
Routine light microscopy and transmission and scanning electron microscopy were used to describe and compare the livers of larval lampreys, Lampetra lamottenii before and during infection of the bile ducts by the nematode, Truttaedacnitis stelmioides. The hepatocytes of uninfected animals differ from other lamprey species in that they contain abundant glycogen, smooth endoplasmic reticulum (SER), and lipoprotein indicating that the liver may be involved in glucose metabolism. Infestation of the biliary tree by T. stelmioides coincides with alterations to the hepatocytes. These changes include dilation of the bile canaliculi, smooth endoplasmic reticulum (SER), rough endoplasmic reticulum (RER), and Golgi apparatus, swollen mitochondria in cells showing a high degree of hypertrophy, and an abundance of dense bodies. Following infection, the sinusoidal lumina became dilated and contain a moderate electron-dense precipitate, an abundance of melanomacrophages, lipocytes, and mononuclear cells. There is also a widening of the fenestrae of the sinusoidal endothelium following infection. Many of the changes in hepatocytes and sinusoids following parasite infections closely resemble those observed in hepatocytes in various pathologies and following experimental bile duct ligation and, therefore, are likely a consequence of increased biliary pressure due to bile duct obstruction. Topics: Animals; Biliverdine; Cholestasis; Cytoplasm; Glycogen; Lampreys; Larva; Liver; Nematode Infections | 1992 |
[Hepatic tissue respiration in pathology of the biliary system and the effect of hyperbaric oxygenation on the course of hepatic insufficiency].
Under study was the effect of hyperbaric oxygenation in 46 patients on the course of bile tract diseases, complicated with hepatic insufficiency. Hyperbaric oxygenation was found to render a positive effect on the course of hepatic insufficiency. Topics: Acid Phosphatase; Acute Disease; Aged; Alkaline Phosphatase; Cholecystitis; Cholestasis; Chronic Disease; Electron Transport Complex IV; Female; Glycogen; Humans; Hyperbaric Oxygenation; Liver; Male; Middle Aged; Oxygen Consumption; Succinate Dehydrogenase | 1976 |
Synthetic capacity and cell metabolites of bile duct obstructed rat livers. Effect of free and conjugated dihydroxy bile acids.
Morphologic alterations in liver cells after bile duct ligation are well known and documented in numerous reports. Biochemical studies concerning metabolic changes in cholestatic liver are rare. Therefore, in this study, liver cell metabolites and the capacity of the perfused cholestatic rat liver to produce glucose, urea and ketone bodies were measured. In addition the influence of dihydroxy bile acids on normal and bile duct ligated rat livers was studied. Concentrations of adenine nucleotides, lactate, pyruvate, 3-hydroxybutyrate, acetoacetate, glucose and UDP-glucose were found to be identical in cholestatic and normal livers. Glycogen content, however, was significantly lowered in cholestatic livers. Gluconeogenesis from lactate and urea production from ammonium chloride were only slightly reduced in bile duct obstructed rat livers. Dihydroxy bile acids did not affect the metabolism of normal or cholestatic livers. Ketone body production from oleate was reduced to 66% in bile duct obstructed livers, taurochenodeoxycholate further reduced this value to the normal value. In contrast to earlier reports (Fisher and co-workers, 1971 Lab. Invest. 21; 88-91; Gastroenterology 60: 742) chenodeoxycholate induced neither cholestasis nor a marked fall in ATP content or rat liver in our experiments with female Wistar rats. In conclusion, dihydroxy bile salts did exert toxic short term effects on rat livers. Topics: Acetoacetates; Adenine Nucleotides; Animals; Chenodeoxycholic Acid; Cholestasis; Cholic Acids; Common Bile Duct; Deoxycholic Acid; Female; Gluconeogenesis; Glycogen; Hydroxybutyrates; Ketone Bodies; Ligation; Liver; Male; Rats; Urea | 1975 |
Ultrastructural changes in the biliary tracts of guinea-pigs infected with Clonorchis sinensis.
Topics: Animals; Basement Membrane; Bile Ducts; Biliary Tract; Cell Nucleus; Cholestasis; Clonorchiasis; Cytoplasm; Cytoplasmic Granules; Endoplasmic Reticulum; Eosinophils; Epithelium; Fibroblasts; Glycogen; Guinea Pigs; Microscopy, Electron; Mitochondria; Mucins; Organoids; Ribosomes | 1973 |
Quantitative changes in liver-cell organelles in cholestasis.
Topics: Biopsy; Cholestasis; Endoplasmic Reticulum; Glycogen; Humans; Hyperbilirubinemia, Hereditary; Liver; Microscopy, Electron; Mitochondria, Liver; Organoids | 1972 |
[Experimental biliary tract occlusion and carbohydrate reserves of the liver].
Topics: Animals; Carbohydrate Metabolism; Cholestasis; Common Bile Duct; Glycogen; Liver; Rats | 1965 |