Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

A recently developed method for the (quantitative) demonstration of glucose-6-phosphate dehydrogenase activity in individual cells with the use of a polyacrylamide carrier has been extended for other enzyme cytochemical techniques. Isolated hepatocytes have been incorporated in the matrix of a thin transparent polyacrylamide gel prior to incubation in a cytochemical medium. The techniques which have been applied are the synthetizing reaction technique for glycogen phosphorylase, the indigogenic method for nonspecific esterase, the metal salt method for glucose-6-phosphatase, the post-azo-coupling technique for acid phosphatase, and the tetrazolium salt technique for succinate and lactate dehydrogenase activities. In all cases a few major problems which occur in the cytochemistry on single cells seem to be solved. The morphology is very well preserved, the final reaction product seems to be precipitated at the expected site of enzyme activity and the coloured end-product is highly specific for the enzyme activity to be studied, as has been demonstrated well with control experiments. The conclusion is reached, therefore, that this relatively simple device can be used routinely for the optimalization of enzyme cytochemistry of single cells.
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PMID:Enzyme cytochemical staining of individual cells with the use of a polyacrylamide carrier. Studies on the synthetizing reaction technique, the indigogenic method, the metal salt method, the post-azo-coupling technique, and the tetrazolium salt technique. 619 80

The effects of diabetes on hepatic carbohydrate metabolism were investigated in spontaneously diabetic Bio-Breeding Worcester (BB/W) rats. The juvenile-onset-type syndrome displayed by these animals is characterized by beta-cell destruction with subsequent ketosis-prone insulinopenia. Livers from diabetic animals demonstrated increased adenosine 3',5'-cyclic monophosphate levels but subnormal total protein and glycogen content. Isolated perfused livers of diabetic BB/W rats demonstrated an increased rate of glucose production from [14C]lactate and an impaired rate of glycogen synthesis. These data were consonant with hepatic enzyme studies demonstrating markedly increased activities of component gluconeogenic (glucose-6-phosphatase, fructose-1,6-diphosphatase, phosphoenolpyruvate carboxykinase) and glycogenolytic (glycogen phosphorylase) enzymes with decreased activities of glycolytic (hexokinase, pyruvate kinase) and glycogenic (glycogen synthase) enzymes. These findings agree with previous studies using alloxan- and streptozotocin-induced diabetic animals and suggest that accelerated hepatic gluconeogenesis and impaired glucose utilization are pathognomonic of all insulin-deficient diabetic syndromes.
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PMID:Hepatic carbohydrate metabolism in the spontaneously diabetic Bio-Breeding Worcester rat. 625 45

The livers from a total of 51 Sprague-Dawley rats treated with different doses of N-nitrosomorpholine (80-120 mg/l in the drinking water) for up to 14 weeks together with the livers of 28 control animals were histochemically investigated at the cessation of carcinogenic insult and at varying periods thereafter for their glycogen content, basophilia and activities of various enzymes of carbohydrate metabolism: glycogen synthetase, glycogen phosphorylase, glucose-6-phosphatase, glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase. The enzymatic patterns of normal tissue, preneoplastic and neoplastic lesions were characterized and compared with reference to the morphologically defined stages of tumor development in the liver. The early appearing glycogen storing areas, localized in the peripheral and intermediate lobular regions, did not show significant changes in the histochemically demonstrable activities of the enzymes tested. After cessation of the carcinogen treatment the more pronounced glycogen storage foci which developed within the aforementioned regions of the liver acinus usually showed a reduction in the activities of phosphorylase and glucose-6-phosphatase while the activity of glucose-6-phosphate dehydrogenase, a key enzyme for the pentose phosphate pathway, was increased. The mixed cell foci, neoplastic nodules and tumors which emerged at later stages were characterized by a progressive shift away from glycogen metabolism towards glycolysis and the pentose phosphate pathway, as indicated by an increase in glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase activities. These changes in enzyme pattern are supportive of a developmental sequence leading from glycogen storage foci through mixed cell foci and neoplastic nodules to hepatocellular carcinomas.
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PMID:Correlative histochemistry of some enzymes of carbohydrate metabolism in preneoplastic and neoplastic lesions in the rat liver. 629 53

Sprague-Dawley rats were treated with N-nitrosomorpholine (NNM) alone (7 weeks, 120 mg/l in drinking water), with NNM followed by phenobarbital (PB) (750 mg/l for 6 weeks) or PB alone. The livers from these animals were investigated for glycogen content and activities of glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, glycogen phosphorylase and glycogen synthetase. The following parameters proved to be significantly altered in the livers of rats treated with either NNM or PB or both compared with untreated controls: glycogen content was increased and the activities of glucose-6-phosphatase and glycogen synthetase were decreased. Although these data show some similarities in changes of glycogen metabolism of livers treated with NNM or PB, earlier histochemical investigations revealed important differences in the distribution of these alterations within the liver parenchyma.
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PMID:Influence of phenobarbital on glycogen metabolism of rat liver pretreated with N-nitrosomorpholine. 630 40

Systematic studies of the sequence of cellular changes during hepatocarcinogenesis induced predominantly in rats by stop experiments with N-nitrosomorpholine (NNM) led to the following main results and conclusions: The development of hepatocellular tumors is preceded by a multifocal hepatic glycogen storage disease (glycogenosis). Cytomorphological and cytochemical findings suggest a sequence of focal changes leading from clear and acidophilic glycogen storage foci through mixed cell foci and neoplastic nodules to hepatocellular carcinomas. The clear and acidophilic glycogen storage cells persisting after withdrawal of the carcinogen apparently represent a preneoplastic cell population, the neoplastic transformation of which is accompanied by a gradual reduction of glycogen and a concomitant increase in ribosomes (basophilia). The first appearance and frequency of the different liver lesions investigated was shown to depend on the dose of carcinogen administered. With increasing dose of NNM, the number of focal lesions considerably increased, and this was accompanied by an earlier development of mixed and basophilic cell populations. There was no indication of any reversibility of pronounced focal lesions under the experimental conditions chosen. On the contrary, the foci became larger and acquired phenotypic markers closer to neoplasia independent of further action of the carcinogen. Enzyme histochemically, the majority of the pronounced glycogen storage foci showed a reduction in the activities of glycogen phosphorylase and glucose-6-phosphatase while the activity of glucose-6-phosphate dehydrogenase, a key enzyme for the pentose phosphate pathway, was increased. The mixed cell foci, neoplastic nodules and carcinomas which emerged at later stages were characterized by a progressive shift away from glycogen metabolism towards glycolysis and the pentose phosphate pathway. as indicated by an increase in glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase activities. These changes in enzyme pattern are in keeping with a developmental sequence leading from glycogen storage foci through mixed cell foci and neoplastic nodules to hepatocellular carcinomas. Biochemical microanalysis of dissected glycogen storage foci and mixed cell foci revealed that the foci composed exclusively of storage cells contained on an average 100% more glycogen than the normal liver tissue. The overall glycogen content of the mixed cell foci, which were composed of both glycogenotic and glycogen-poor basophilic cells, was not distinguishable from that of normal tissue.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepatocellular glycogenosis and related pattern of enzymatic changes during hepatocarcinogenesis. 659 71

Glycogen synthase, glycogen phosphorylase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and glucose-6-phosphatase were determined for the first time in the necessary lobes of Lachi from late embryonic chicks. The activities of these enzymes were compared with those found in other glycogen-metabolizing tissues, specifically the glycogen body, liver, and skeletal muscle, obtained from the same embryos. The data show that, as in the glycogen body, the accessory lobes of Lachi lack glucose-6-phosphatase, but contain relatively high activity levels of glycogen synthase I, total and active glycogen phosphorylase, and the dehydrogenases of glucose-6-phosphate and 6-phosphogluconate. The percent of glycogen synthase I activity in the Lachi lobes is from two- to 20-fold greater than observed in the glycogen body, liver, or muscle, whereas the percent of glycogen phosphorylase a activity is comparable to that of the liver, but greater than that in the glycogen body or muscle. The activity of each dehydrogenase of the pentose phosphate cycle in the Lachi lobes is similar to that noted in the glycogen body, but is over two- or fivefold greater than that activity found in muscle or liver. Our data, together with other recent evidence, suggest that the role of glycogen in these functionally enigmatic tissues may be to support the precocious process of myelin synthesis in the developing bird, as well as possibly to provide alternate sources of energy for the avian central nervous system.
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PMID:Glycogen metabolism in the developing accessory lobes of Lachi in the nerve cord of the chick: metabolic correlations with the avian glycogen body. 678 75

Optimum conditions were established for the assay of glycogen, glycogen synthase, glycogen phosphorylase, phosphoglucomutase, and glucose-6-phosphatase in rabbit fetal heart, lung, and liver. Using these methods, the pattern of appearance of glycogen and the above four enzymes was established from day 18 of gestation to day 8 after birth. The results indicate that total tissue glycogen reaches maximum levels between days 22 and 24 in the heart, days 24 and 26 in the lung, and days 30 and 31 in the liver. In all three tissues, the rapid rise or depletion of glycogen is coincident with a corresponding increase in glycogen synthase and glycogen phosphorylase activities. However, substantial amounts of glycogen synthase are present both prior to and after the accumulation of glycogen. Similarly, considerable amounts of glycogen phosphorylase are present early in gestation, yet deposition of glycogen occurs. Both the I and D forms of glycogen synthase are present in the three tissues, the major being the physiologically inactive D form. Similarly both the a and b forms of glycogen phosphorylase are present, with the a form (active form) making up about 30-60% of the total phosphorylase activity. Glucose-6-phosphatase was absent in fetal heart and lung throughout the period of gestation investigated. Low levels of this enzyme were detectable in fetal liver near term. The phosphoglucomutase activity increased progressively from day 22 of gestation in all three tissues and continues to increase after birth. The disappearance of fetal lung glycogen occurs between days 27 and 28 at a time when surfactant phospholipids first appear. These findings indicate that the breakdown of glycogen is providing the fetal lung cells with energy necessary for surfactant phospholipid biosynthesis.
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PMID:Ontogeny of some enzymes of glycogen metabolism in rabbit fetal heart, lungs, and liver. 685 Apr 15

A comparative morphologic, morphometric and enzyme histochemical investigation of lesions induced by short-term application of N-nitrosomorpholine (NNM) and subsequent so-called 'selection pressure' was carried out in order to assess the characteristics of the numbers of induced putative preneoplastic populations and to cast light on reversibility associated with this model. The glycogen storage foci, mixed cell foci and neoplastic nodules observed after 'selection pressure' were in principle similar to those seen after stop experiments, although alterations in morphology and enzyme phenotype of individual cells were usually far more pronounced after short-term induction. It was established that 75% of the lesions were no longer visible 11 weeks after withdrawal of induction stimuli and that a large proportion of these remaining demonstrated heterogeneity in morphological and histochemical markers indicative of reversion to normal phenotype. After a further 10 weeks a slight increase in number of foci associated with decrease in size and enhanced homogeneity in phenotypic markers was established. The behaviour of foci and nodules undergoing reversion was considered with respect to changes in basophilia and glycogen storage and activity of the enzymes glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, glyceraldehyde 3-phosphate dehydrogenase, glycogen phosphorylase and synthase, acid phosphatase and gamma-glutamyl transpeptidase and correlated with location of altered cellular populations within the liver functional acinus.
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PMID:Phenotypic instability in focal and nodular lesions induced in a short term system in the rat liver. 685 Sep 91

The livers of rats treated for 12 weeks with N-nitrosomorpholine (80 mg/1 drinking water) were investigated on the day of carcinogen withdrawal (12 + 0 weeks) and 8 weeks after cessation of treatment (12 + 8 weeks). The glycogen content in relation to the DNA and protein content of the liver and the activities of glycogen synthetase, glycogen phosphorylase, glucose-6-phosphatase, and glucose-6-phosphate dehydrogenase were determined in the liver homogenates. The glycogen content of the livers was slightly elevated at both times investigated. Phosphorylase and synthetase activities showed no clear alterations in livers of treated animals as compared with controls. Glucose-6-phosphatase activity was significantly reduced at 12 + 0 weeks and returned to normal values at 12 + 8 weeks. The activity of glucose-6-phosphate dehydrogenase was unchanged at 12 + 0 weeks, but exhibited a significant increase at 12 + 8 weeks. Polyacrylamide gel electrophoresis with staining of the gels by an assay specific for the glucose-6-phosphate-dehydrogenase-catalysed reaction revealed the same pattern of active bands in treated and untreated animals but with higher activities in two bands originating from extracts of nitrosomorpholine-treated livers.
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PMID:Biochemical correlation of glycogen content and activity of some enzymes of carbohydrate metabolism in rat liver during early stages of carcinogenesis. 713 Feb 54

The effect of daily intraperitoneal administration of Mn2+(4 mg/kg) was investigated on the metabolism of carbohydrates and certain enzymes involved in the oxidation of glucose in the rat liver and blood at the intervals of 30, 60 and 90 days after exposure. Mn2+ had no effect on the contents of blood reducing sugars and proteins, however the levels of pyruvic and lactic acids were reduced at 60 and 90 days after the metal treatment. The contents of liver glycogen and proteins remained unaffected while pyruvic acid content was decreased in Mn2+ treated rat liver throughout the experimental period. The activities of glycogen phosphorylase and lactate dehydrogenase decreased while that of phosphoglucoisomerase and glucose-6-phosphatase increased in the post mitochondrial supernatant at 60 and 90 days of Mn2+ exposure. The levels of hexokinase decreased and FDP-aldolase and fructose-1, 6-diphosphatase increased throughout the experimental period. The magnitude of alteration was found to be greater with the increase in the duration of Mn2+ treatment. Several of the mitochondrial enzymes in the liver were inhibited in the manganese exposed rats which may be responsible to inhibit the rate of dehydrogenation of Kreb cycle's intermediates along with the linked respiratory chain and eventually oxidation in the rat liver.
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PMID:Effects of manganese on carbohydrate metabolism and mitochondrial enzymes in rats. 713 26


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