Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phosphorylase activities (total and a form) were determined in the livers of experimental hepatic injuries with carbon tetrachloride or galactosamine and the livers of patients with liver diseases. Experimental liver injuries caused a slight decrease in total activity in later stages and a marked increase in a form activity in earlier stages. In human livers, low values of total activity were found in acute hepatitis and cirrhosis of the liver with no consistent alteration in a activity. Phosphorylase activities in hepatocellular carcinomas were also low. The importance of the altered phosphorylase activities in hepatic injuries is discussed in relation to the disorder in glycogen metabolism in the injured liver.
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PMID:Studies of liver phosphorylase in hepatic injuries. I. Alteration in enzyme activity. 15 88

Enzyme deviations in injured livers were studied by analyzing isozyme patterns of phosphorylase using a newly developed electrophoretic method, which separates six molecular species of this enzyme, i.e. M,FM,F,L,L', and FL'. In hepatic injuries caused by CCl4 and galactosamine intoxications of rats, F appeared in early stages and L' (and FL') in later stages of the injuries with a concurrent decrease or loss of L, which is a sole isozyme component of adult liver. In injured livers of patients with hepatitis and cirrhosis of the liver, increases in FL' activity were also found. Appearance of F was found only in hepatocellular carcinoma. The results obtained with phosphorylase isozyme analysis support the idea that an undifferentiated gene expression takes place in the injured livers of non-malignant hepatic disorders.
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PMID:Studies of liver phosphorylase in hepatic injuries II. Alteration in isozyme pattern. 15 93

By cytofluorometric method, a study was made of the total glycogen and its two fractions in liver parenchymal cells both in the donors (20 men) and in patients with cirrhosis of different etiology (39 men). The examination was performed on preparations--smears of isolated hepatocytes, obtained from the live functional liver biopsies. The quantitative analysis has shown an increase in the total glycogen content in hepatocytes of patients with cirrhosis by 3 times compared to the norm, and this increase is independent on the etiology of liver cirrhosis. To study the mechanism of the discovered glycogenosis, the activity of key enzymes of glycogenolyses was determined. It was shown that glucose-6-phosphatase and glycogen-phosphorylase activity in the liver with cirrhosis was lower than in the norm. The most considerable changes were shown in hepatocytes of patients with liver cirrhosis in fractional glycogen composition and, even more significant, in the content of a hard soluble fraction. The hard soluble fraction portion was higher in hepatocytes of the patients with liver cirrhosis of alcohol etiology. The quantitative analysis of glycogen fraction contents in liver cells may be the best marker in the differential diagnosis of symptomless elapsing liver cirrhosis.
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PMID:[Cytofluorimetric research on the content of glycogen and its fractions in the hepatocytes of patients with liver cirrhosis of different etiologies]. 130 90

Glucose homeostasis and fatty acid metabolism are abnormal in patients with cirrhosis. To assess the metabolic response to starvation in an animal model of cirrhosis, glycogen and fuel metabolism were characterized in rats with CCl4-induced cirrhosis studied 2 wk after 10 weekly doses of CCl4. Plasma concentrations of glucose and beta-hydroxybutyrate were not different between fed CCl4-treated and control rats, but plasma nonesterified fatty acid concentrations were higher in cirrhotic animals (0.25 +/- 0.01 vs. 0.39 +/- 0.04 mmol/L; p less than 0.05). After 12 hr of starvation, the plasma nonesterified fatty acid concentration had reached 0.58 +/- 0.04 mmol/L in CCl4-treated rats, compared with 0.38 +/- 0.04 mmol/L in control rats (p less than 0.05). The redistribution of the hepatic carnitine pool toward acylcarnitines, which is characteristic of starvation, was complete after fasting for 12 hr in the CCl4-treated rats, compared with the 24 hr required in control rats. In fed cirrhotic rats, liver glycogen content per gram liver was decreased by 64% compared with control rats (30.0 +/- 5.1 vs. 10.8 +/- 1.1 mg/gm liver wet wt; p less than 0.05). After 12-hr fasting, hepatic glycogen content had fallen to 14.3 +/- 3.9 and 4.8 +/- 0.4 mg/gm liver wet wt (p less than 0.05) in control and cirrhotic animals, respectively. To further characterize the status of glycogen metabolism in cirrhotic livers, activities of glycogen synthase and glycogen phosphorylase were determined. Hepatic active and total glycogen phosphorylase activities normalized to hepatocellular content were unaffected by CCl4 treatment, whereas total glycogen synthase activity was increased by 45%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased hepatic glycogen content and accelerated response to starvation in rats with carbon tetrachloride-induced cirrhosis. 195 69

Type IV glycogenosis is due to branching enzyme deficiency and is usually manifested clinically by progressive liver disease with cirrhosis and hepatic failure between the second and fourth years of life. We describe a 5-year-old boy who, following an acute febrile illness at 2 years of age, was first noted to have hepatomegaly with mildly elevated serum transaminase levels. Liver biopsy revealed hepatic fibrosis with periodic-acid Schiff-positive, diastase-resistant inclusions in hepatocytes and fibrillar inclusions characteristic of amylopectin by electron microscopy. Enzymatic assay revealed deficient hepatic branching enzyme activity with normal activity of glucose-6-phosphatase, debranching enzyme and phosphorylase activities. During the succeeding 3 years, he grew and developed normally with apparent resolution of any clinical evidence of liver disease and only intermittent elevation in serum transaminase levels associated with fever and prolonged fasting. Repeat liver biopsy at 4 years of age showed persistence of scattered hepatocellular periodic-acid Schiff-positive, diastase-resistant inclusions, but no progression of hepatic fibrosis in spite of persistent deficiency of hepatic branching enzyme activity. Skeletal muscle and skin fibroblasts from the patient also showed deficient enzyme activity. Skin fibroblasts from both parents exhibited half the normal control activity, suggesting a heterozygote state. This is the first documented patient with deficiency of branching enzyme but without evidence of progressive hepatic disease. This patient, coupled with reports of other patients with late onset hepatic or muscle disease with branching enzyme deficiency, suggests that the defect resulting in Type IV glycogen storage disease is more heterogenous and possibly more common than previously suspected.
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PMID:A new variant of type IV glycogenosis: deficiency of branching enzyme activity without apparent progressive liver disease. 316 25

Abnormal liver tests, right upper quadrant pain and hepatomegaly occurring in an obese or in a diabetic patient may point to the presence of fat or of glycogen accumulation in the liver parenchymal cells. Marked hepatomegaly due to cytoplasmic glycogen deposition is mainly found in poorly controlled insulin-dependent diabetic patients. If accompanied by cushingoid features, growth retardation and by delayed puberty, a diagnosis of Mauriac syndrome can be made. Hyperglycaemia, insulin administration and increased concentrations of the counterregulatory hormone cortisol may all play a role in the glycogen deposition by their concerted actions on the glycogen phosphorylase and synthase enzymes, promoting the accumulation of glycogen. Hypercortisolism may be responsible for growth retardation and delayed puberty in Mauriac patients. Regression of hepatomegaly and of the associated clinical characteristics may be obtained by a better metabolic control due to the administration of long-acting insulin and the change from single to twice daily injections. Fatty liver is rare in insulin-dependent diabetic patients and is indicative of a poor diabetic control. This process is quickly reversible by adequate insulin treatment. Steatosis is frequently found in maturity-onset diabetics and in obese patients. The pathogenetic mechanisms leading to the accumulation of triglycerides and of fatty acids in the hepatocytes can easily be understood from the normal cycling of fatty acids between the adiopose tissue and the liver. Histologic features of nonalcoholic steatohepatitis can also be found in obese and in diabetic patients. Steatohepatitis may rarely evolve into cirrhosis. In general, there is no correlation between the degree of the biochemical alterations and the severity of the histological findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver disturbances in obesity and diabetes mellitus. 858 Oct 74

The paper deals with a cytofluorimetric study of the content of glycogen and its fractions as well as with a microbiochemical study of glucose-6-phosphatase, glycogen phosphorylase, and glycogen synthase activities in the rat liver parenchyma cells in norm, in the course of cirrhosis development, and at various time intervals after the end of the carbon tetrachloride (CCl4) poisoning and after a partial hepatectomy (PH). Serial liver biopsies were obtained from each animal prior to CCl4 action (control), 6 months after a chronic intoxication with CCl4 inducing liver cirrhosis, and then 3 and 6 months after the end of CCl4 poisoning of rats, and after the cirrhotic liver PH. It has been shown that the total glycogen content in the cirrhotic liver hepatocytes increases by 1.4-1.5 times, compared with control, however, it returns to the norm 6 months after the PH. The glycogen labile fraction (LF), that accounts for 85% of the total glycogen, amounted to 65% in liver cirrhosis. The most striking changes in liver cirrhosis occurred in the glycogen stable fraction (SF) which rose by 3.9 times in the cirrhotic liver. The LF/SF ratio returned to the norm 6 months after the PH. The activity of glucose-6-phosphatase fell by 2.7 times in the liver cirrhosis; its activity after the PH initially increased, then decreased again to reach 6 months after the PH the same level as in the cirrhotic liver before the PH. The activities of glycogen phosphorylase and glycogen synthase returned to the normal level 6 months after the PH. The results of the current study make it possible to conclude that the PH of the cirrhotic liver facilitates only a partial restoration of the glycogen forming function of hepatocytes.
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PMID:[The glycogen-forming function of the hepatocytes during the regeneration of the cirrhotic rat liver after a partial hepatectomy]. 901 96

By cytofluorometric and biochemical methods the content of total glycogen and its fractions was investigated on the smears of isolated liver cells: labile fraction (LF) and stable fraction (SF) and also activities of glycogen phosphorylase (GP), glucose-6-phosphatase (G-6-Pase) and glycogen synthase. The material was obtained from serial liver biopsies from each investigated animal prior to CCl4 action (control), with cirrhosis (6 months of CCl4 poisoning) and 1, 3 and 6 months after CCl4 poisoning was finished. It was shown that chronic CCl4 poisoning induced a typical liver cirrhosis accompanied with the 2-3 times increase in the total glycogen content, in comparison with the norm, with the decrease in LF to 53%, and also with the fall of G-6-Pase and GP activities by 82 and 25%, resp. After 1, 3 and 6 months following poisoning cessation, the lobule structure, infringed due to cirrhosis, was not restored. But functional parameters of the cirrhotic liver were seen gradually recovering without CCl4 poisoning. The application of carbohydrate rich diet favoured a most complete rehabilitation: the content of total glycogen and its fractions and the activity of G-6-Pase and GP returned to the normal level.
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PMID:[Rehabilitation of the hepatocyte glycogen-forming function in the rat cirrhotic liver due to carbohydrate rich diet]. 961 Apr 78

Rat liver punctate biopsies were used for cytofluorimetric determinations of the content of glycogen and its fractions in hepatocytes, and also for microchemical measurements of the activity of glucose-6-phosphatase, glycogen phosphorylase, and glycogen synthase, in liver tissue with cirrhosis produced by carbon tetrachloride (CCl4) poisoning, during regeneration of the liver after the cessation of poisoning and after a partial resection of the cirrhosed liver. The liver cirrhosis was shown to be characterized by an accumulation of glycogen (predominantly of its metabolically less active fraction) in hepatocytes and by a decrease in the activities of the glycogenolytic enzymes in the liver parenchyma. On the cessation of poisoning, there was a partial or complete return to normal levels of the glycogen metabolism parameters. Some of them returned to normal more quickly if a partial hepatectomy was performed after the cessation of poisoning.
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PMID:Glycogen-forming function of hepatocytes in the rat regenerating cirrhotic liver after a partial hepatectomy. 966 Dec 97

Using rat liver hepatocytes, methods of cytofluorimetry (Kudryavtseva et al., 1974) and biochemistry were applied to comparative studies of the total glycogen content, including its labile (LF) and stable (SF) fractions, and activities of glucose-6-phosphatase, glycogen phosphorylase and glycogensynthetase in these. The liver hepatocytes were examined in norm, and under conditions of CCl4 poisoning of rats, both 6 months after a chronic poisoning, and 1, 3 and 6 months following poisoning cessation. All the experimentally poisoned rats were divided into two conventional groups: rats of one group received, apart from poisoning, a complex treatment with chorionic gonadotropin (CG); the other group rats received, no treatment. The material used for examination was obtained from serial functional biopsies of each experimental animal. It has been shown that under cirrhosis the content of the total glycogen in hepatocytes increased by 3 times, and that of its SF even by 9.7 times. The treatment with CG for 1 month resulted in its reducing to the norm, and 3 to 6 months treatments normalized contents of both the glycogen fractions. In the group of non-treated rats no similar changes were registered. Besides, in the cirrotic rats the activity of glucose-6-phosphatase was shown to increase by 4 times. After CG treatment it was seen to decrease by 3 times. Thus, CG may be regarded as an optimum and more effective agent for restoring abnormalities in cirrotic liver, compared to some other stimulating factors, such as hepatectomy (Kudryavtseva et al., 1996) or rich-carbohydrate diet (Kudryavtseva et al., 1998).
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PMID:[Glycogen synthesizing function of hepatocytes in rats with liver cirrhosis after treatment with chorionic gonadotropin]. 1050 31


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