Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of hexokinase (HK), its isoenzymes, glucose-6-phosphatase and glucose-6-phosphate dehydrogenase, and the triiodothyronine (T3) effect on this activity in the liver tissue of mice bearing transplantable hepatoma 22a were studied in different periods of the tumor growtn. It was shown that alterations in the activity of the enzymes in the liver of tumor-bearing mice occurred already in the presence of a small tumor. More profound alterations in the activity of all enzymes studied, apart from those in the enzymatic pattern of HK, could be observed starting from day 21after the tumor transplantation. In the initial stages of the hepatoma growth the activity of the test enzymes in the liver was regulated by thyroid hormone. The effect of Ta on the activity of the enzymes in the host liver was gradually lost in the course of the tumor growth.
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PMID:[Carbohydrate metabolism enzymatic activity and its alteration under the influence of thyroid hormone during tumor growth]. 22 89

The disorder of gene expression in hepatomas was studied by following certain metabolic alterations (enzyme stimulation, nucleic acid labeling) after glucocorticoid treatment and analyzing the site of action of glucocorticoids. Compared to normal liver, the MC-29 virus-derived transplantable hepatoma (VTH) responded abnormally to glucocorticoids, which failed to stimulate the activity of certain enzymes (glucose-6-phosphatase, aryl hydrocarbon hydroxylase) or to inhibit DNA synthesis. Since the binding capacity of the cytosol steroid receptor was the same in liver and VTH but the interaction between the steroid receptor and DNA was reduced in VTH, it was concluded that structural alterations of chromatin nonhistones--including processed steroid receptor--may be responsible for the lack of physiological responses to steroids in VTH. Furthermore, the increased proportion or repetitive sequences in VTH DNA may be a feature of the disorder of gene regulation in malignant cells.
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PMID:Chromatin alterations and gene function disorder in MC-29 virus-derived hepatoma. 22 7

The ability of liver lipid-exchange proteins to introduce foreign phospholipids into microsomes was used in a study of the lipid dependence of glucose-6-phosphatase. Supplementation of intact rat liver and hepatoma microsomes with exogeneous aminophospholipids prevents the decline of glucose-6-phosphatase activity during incubation, whereas the introduction of exogeneous phosphatidylcholine has no protective effect. On the contrary with deoxycholate-disrupted hepatoma microsomes, introduction of additional phosphatidylcholine causes activation while phosphatidylethanolamine has only little effect. The results are explained by assuming that the transport unit and the catalytic moiety of the glucose-6-phosphatase system have different lipid requirements, the activity of the former protein depending mainly on phosphatidylethanolamine and phosphatidylserine and that of the catalytic protein depending on phosphatidylcholine. In deoxycholate-disrupted liver microsomes (in which both the glucose-6-phosphatase activity and the phosphatidylcholine content are much higher than in hepatoma microsomes) incubation with phosphatidylcholine and lipid-exchange proteins alters neither the phospholipid composition nor the enzyme activity. THis suggests that the diminished activity of glucose-6-phosphatase in hepatomas may be partly due to a low level of phosphatidylcholine.
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PMID:Use of protein-mediated lipid exchange in the study of membrane-bound enzymes. The lipid dependence of glucose-6-phosphatase. 22 88

Further biochemical characterization of the Albert hepatoma has been performed. The following results were obtained: In spite of often repeated transplantations and a medium growth rate, the Albert hepatoma does still contain organ-characteristic enzymes. We have found significant activities of glucokinase, glucose-6-phosphatase and arginase, and considerable amounts of noradrenaline and glycogen. In addition, it is capable to respond to humoral stimuli, that is, it differs from most of the other hepatocellular malignomas also in this regard.
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PMID:Activities of organ characteristic enzymes and noradrenaline and glycogen contents in the Albert hepatoma of C57BL mice. 22 50

Dehydroepiandrosterone (DHEA), a C19 adrenal steroid hormone, induces peroxisome proliferation in liver cells and is hepatocarcinogenic in the rat. The present study deals with the phenotypic properties of DHEA-induced liver lesions. A majority of the altered areas (80-87%), neoplastic nodules (> 94%) and hepatocellular carcinomas (HCC, 80-100%) lacked the marker enzymes gamma-glutamyltranspeptidase and placental form of glutathione S-transferase (GSTP). Northern blot analysis of HCC from 4 rats revealed no detectable GSTP mRNA. These HCC, however, showed a marked decrease in the staining of glucose-6-phosphatase and adenosine triphosphatase. These results indicate that the phenotypic properties of liver tumors induced by DHEA and amphipathic carboxylate peroxisome proliferators are similar.
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PMID:Phenotypic properties of liver tumors induced by dehydroepiandrosterone in F-344 rats. 133 91

Tumor uptake of 18F-fluorodeoxyglucose (FDG) was studied by dynamic positron emission tomography (PET) in 23 cases of hepatocellular carcinoma. The metabolic rate constants, K1 to K4, were generated by non-linear least square fitting method. We confirmed that K3 from the PET study significantly correlated with directly measured hexokinase activity of the cancer tissue. The region of HCC always had higher K3 values, which represents the hexokinase activity compared with the non-cancerous region. By FDG images, however, in 50% of cases the cancer region could not be clearly defined from the surrounding noncancerous hepatic tissue. These HCC cases without accumulation of FDG had a high ratio of K4/K3 (K4 represents glucose-6-phosphatase activity), which correlated well with the inverse ratio of FDG accumulating images on PET. According to the PET images which is represented by K4/K3 and the hexokinase activity which is represented by K3, we divided these 23 cases into three groups and retrospectively compared their survival rates. The groups with high K4/K3 (greater than or equal to 0.40) had longer survival than other groups. From the view point of glucose metabolism, the value of K4/K3 calculated from dynamic studies of FDG-PET may represent the functional differentiation of HCC.
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PMID:[Can fluorodeoxyglucose-positron emission tomography evaluate the functional differentiation of hepatocellular carcinoma]. 166 76

The significance of glucose-6-phosphatase (G6P) expression by bile duct-like cells proliferating during hepatocarcinogenesis in the histogenesis of hepatocellular carcinoma is not clear. To this end, we measured the histochemical and biochemical activity of G6P in normal rat liver, and in rat livers in which bile duct-like proliferation was induced by either hyperplastic (bile duct ligation for 14 days or feeding alpha-naphthylisothiocyanate for 28 days) or neoplastic (feeding a choline-devoid diet containing 0.1% ethionine for 60 days) regimens. In normal, hyperplastic, and preneoplastic livers, G6P histochemical activity was confined to the hepatocytes; proliferated bile duct-like cells, like normal bile ducts, did not display visible G6P staining. When the enzyme activity was determined biochemically, however, hydrolysis of glucose-6-phosphate was observed in both parenchymal and nonparenchymal liver cells isolated from all experimental animals. In elutriated nonparenchymal fractions, G6P activity was directly proportional to the number of cells positive for gamma-glutamyl transpeptidase and cytokeratin no. 19 (markers of bile duct cells) and inversely proportional to the number of cells positive for vimentin (marker of mesenchymal cells). These results indicate that, while by light microscopy hepatic G6P histochemical activity is detectable only in the hepatocytes, the biochemical activity is also expressed in proliferating bile duct-like cells. However, the nonparenchymal activity is observed during both neoplastic and hyperplastic liver growth, thus indicating that the presence of this enzyme in bile duct-like cells proliferating during hepatocarcinogenesis should not necessarily be construed as supporting their stem cell nature nor their neoplastic commitment.
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PMID:Distribution of glucose-6-phosphatase activity in normal, hyperplastic, and preneoplastic rat liver. 168 20

The effects of oral fructose on hepatocarcinogenesis were investigated with cytomorphological, cytochemical and stereological methods. Carcinogenesis was induced in male Sprague-Dawley rats by application of N-nitrosomorpholine (NNM) for 7 weeks. Afterwards, the animals received fructose in the drinking water (120 g/l) and food ad libitum (group I) or tap water and food ad libitum (group II). The incidence of hepatocellular carcinoma in rats treated with NNM plus fructose was 46% as compared to 24% in animals receiving NNM alone (P less than 0.05). There was no difference in the incidences of other malignancies between the groups (group I: 32.1%, group II: 32.0%). Morphometric evaluation of preneoplastic liver lesions indicated the enhancing effect of the fructose treatment several months before malignant tumors appeared. As early as 6 weeks after treatment the hepatic parenchyma occupied by focal lesions was increased from 6.7% in the animals which had received NNM alone to 8.5% (P less than 0.05) in animals having received NNM plus fructose. This increase was predominantly caused by an increase in glycogen storing foci (P less than 0.0005). In addition, the fructose treatment caused a histochemically detectable increase in the activity of glucose-6-phosphatase and glucose-6-phosphate dehydrogenase in both the hepatocytes of the focal lesions and the surrounding parenchyma. In the NNM plus fructose group the activity of the glucose-6-phosphatase in the foci was frequently approximately equal to the activity in the parenchyma of untreated controls. The striking increase in the activity of this enzyme in the surrounding hepatocytes, however, still sharply demarcated the lesions. The potential mechanisms by which fructose enhances hepatocarcinogenesis are discussed.
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PMID:Enhancement of hepatocarcinogenesis in rats by dietary fructose. 256 39

A rat hepatoma cell line was established from primary culture using RPMI 1640 without supplements. Hepatomas were induced in rats by 0.06% 3'-methyl-4-dimethylaminoazobenzene. An established cell line, FF101, has been maintained as a monolayer for longer than 34 months and subcultured for 42 passages. The population-doubling time was 78 h. The modal chromosome number was 66. FF101 was transplantable, and morphological examination of the transplanted tumors revealed a mixed type of hepatocellular and cholangiocellular carcinoma. FF101 retained the ability to express tyrosine aminotransferase and glucose-6-phosphatase. Also, FF101 synthesized alpha-fetoprotein. FF101-conditioned medium stimulated DNA synthesis and proliferation of several cell lines such as AH66, K562, and BALB/c3T3. The growth-promoting activity of FF101-conditioned medium was abolished by protease, dithiothreitol, acidic treatment, and heating. Gel filtration of conditioned medium on Sephacryl S-200 disclosed the growth-promoting activity at the molecular size of approximately 60,000 Da, and the isoelectric point (pI) was between 5.5 and 6.5. These results suggest that FF101 synthesizes a novel growth factor which has little specificity in both species and organs.
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PMID:Partial purification of a growth factor synthesized by a rat hepatoma cell line established in serum-free medium. 270 52

The ten-fold increase in glucose-6-phosphatase, previously reported, in 2S FAZA hepatoma cells exposed to dexamethasone, is completely blocked by low concentrations of insulin. At 3 x 10(-10) M insulin, the activity induced by 10(-6) M dexamethasone is reduced by half. The activity of intact microsomes, which reflects translocation of cytoplasmic glucose 6-phosphate into the endoplasmic reticulum, is induced by dexamethasone, but to a lesser extent than the hydrolase. Insulin also prevents this induction.
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PMID:Effect of insulin on the induction by dexamethasone of glucose-6-phosphohydrolase and translocase activities in cultured hepatoma cells. 283 6


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