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)

We have tested the hypothesis that prolonged fetal hypoxemia causes a reduction in glycogenolytic enzyme activities and/or a depletion of fetal glycogen stores. We compared the effects of short (4 h) and prolonged (24 h) periods of reduced maternal uterine blood flow (RUBF) on glycogen content and on the activities of glucose-6-phosphatase (G-6-Pase), glycogen phosphorylase (GPase), and glycogen synthase (GSase) in selected fetal tissues. RUBF was reduced in 10 pregnant sheep at 135 days of gestation (term approximately 146 days) for either 4 h (n = 5) or 24 h (n = 5); 5 other fetuses were used as controls. During RUBF, fetal SaC2 was decreased from 61.6 +/- 3.9 to 22.0 +/- 1.4% at 4 h and to 26.7 +/- 1.2% at 24 h. Hepatic glycogen content was significantly reduced at 4 h of RUBF, but was not reduced further at 24 h. Fetal liver GPase (active and total enzyme activity) and G-6-Pase activities were reduced at 4 h of RUBF but tended to return toward control values at 24 h. Similarly, hepatic GSase activity tended to decrease at 4 h of RUBF, although the reduction was not quite significant (P = 0.08). We conclude that RUBF causes a reduction of fetal glycogen stores and a reduction in G-6-Pase and GPase activity at 4 h. Fetal tissue glycogen contents were not reduced further at 24 h, compared with 4 h of RUBF, which indicates that fetal glycogenolysis is reduced during this time, probably because of the inhibition of GPase and G-6-Pase. It is not known why the activities of these enzymes are reduced during prolonged RUBF, when circulating epinephrine and norepinephrine concentrations are high.
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PMID:Effect of hypoxemia on tissue glycogen content and glycolytic enzyme activities in fetal sheep. 903 97

Cultured astroglial cells are able to utilize the monosaccharides glucose, mannose, or fructose as well as the sugar alcohol sorbitol as energy fuel. Astroglial uptake of the aldoses is carrier-mediated, whereas a non-saturable transport mechanism is operating for fructose and sorbitol. The first metabolic step for all sugars, including fructose being generated by enzymatic oxidation of sorbitol, is phosphorylation by hexokinase. Besides glucose only mannose may serve as substrate for build-up of astroglial glycogen. Whereas glycogen synthase appears to be present in astrocytes as well as neurons, the exclusive localization of glycogen phosphorylase in astrocytes and ependymal cells of central nervous tissue correlates well with the occurrence of glycogen in these cells. The identification of lactic acid rather than glucose as degradation product of astroglial glycogen appears to render the presence of glucose-6-phosphatase in cultured astrocytes an enigma. The colocalization of pyruvate carboxylase, phosphenolpyruvate carboxykinase and fructose-1,6-bisphosphatase points to astrocytes as being the gluconeogenic cell type of the CNS.
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PMID:Metabolic pathways for glucose in astrocytes. 929 44

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

Using cytofluorimetric and biochemical methods, the content of glycogen and its labile and stable fractions, as well as activities of glucose-6-phosphatase (EC 3.1.3.9), glycogen phosphorylase (EC 2.4.1.1) and glycogen synthase (EC 2.4.1.11) were determined in the rat liver for 6 months after chronic poisoning of the animals with CCl4 and then at 1, 3, and 6 months after the end of the poisoning. One group of rats was given a standard diet, the other, a high-carbohydrate diet. The 6-month long chronic intoxication with CCl4 was shown to produce development of typical liver cirrhosis characterized by a 2.8-fold increase in the total glycogen content in hepatocytes as compared with normal cells, by a fall in the glycogen labile fraction (from 85 to 53% of the total glycogen) as well as by decreases in the activities of glycogen phosphorylase and glucose-6-phosphatase by 25 and 82% respectively. The structural rehabilitation occurred faster and more completely at the cellular level than at the tissue level. Functional variables of the cirrhotic liver tissue also recovered, after cessation of poisoning, faster and more completely than the liver structure at the tissue level: glycogen levels in hepatocytes fell dramatically, the labile: stable glycogen fraction ratio recovered completely, and the activity of glycogen phosphorylase rose to the level characteristic of the normal liver. Use of the high-carbohydrate diet promoted a somewhat faster and more complete recovery of hepatic structure and function.
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PMID:Restoration of the glycogen-forming function of hepatocytes in rats with liver cirrhosis is facilitated by a high-carbohydrate diet. 1061 23

The thyroid hormone 3,5,3'-triiodo-L-thyronine (T3) is a strong direct hepatocyte mitogen in vivo. The effects of T3 resemble those of peroxisome proliferators, which are known to induce hepatocellular tumors in rats. With the aim of studying long-term local effects of thyroid hormones on liver parenchyma, small pieces of thyroid tissue were transplanted via the portal veins into the livers of thyroidectomized male Lewis rats. At 1 week, 3 weeks, 3 months, and 18 months after transplantation, the transplants were found to proliferate, to synthesize thyroglobulin, and to release thyroxine and T3. At 3 and 18 months after transplantation, the hepatocytes of the liver acini downstream of the transplanted follicles showed an increase in cytoplasmic basophilia, a loss of glycogen, an enlargement and hyperchromasia of their nuclei, and a strong increase in cell turnover compared with unaltered liver acini. The altered hepatocytes exhibited an increase in the activities of glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, malic enzyme, mitochondrial glycerol-3-phosphate dehydrogenase, cytochrome-c-oxidase, and acid phosphatase; the activities of glycogen synthase and glycogen phosphorylase were strongly decreased. The hepatocytic alterations downstream of the transplanted follicles could be explained by effects of T3. On the other hand, they resembled alterations characteristic of amphophilic preneoplastic liver foci observed in different models of hepatocarcinogenesis.
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PMID:Hyperproliferative hepatocellular alterations after intraportal transplantation of thyroid follicles. 1062 58

Effects of a dipeptide preparation "Vilon" on rehabilitation of functional activity of hepatocytes and regeneration of the cirrhotically altered rat liver were studied. The liver cirrhosis was produced by poisoning of rats for 4 months with carbon tetrachloride (CCl4). On the end of the poisoning with CCl4, one group of animals was not submitted to any further actions, whereas animals of the other group were injected "Vilon" (1.7 micrograms/kg) daily for 5 days. On smears of isolated hepatocytes, contents of total glycogen (TG), and its labile and stable fractions (LF and SF) were determined in addition to cell ploidy levels and the total protein content. In liver homogenates, activities of glucose-6-phosphatase (G6P), glycogen synthase (GS), and glycogen phosphorylase (GP) were measured. In 2 weeks after the drug application, G6P activity being reduced in cirrhosis 1.2 times, elevated under effect of "Vilon". In non-treated rats the contents of TG and its fractions and of G6P activity remained at the level characteristic of the cirrhotic liver prior to "Vilon" administration. In both groups of rats, GP and GS activities in the cirrhotically altered liver did not differ from their control values throughout the entire experiment. "Vilon" has been shown to exert a weak stimulating effect on regeneration of the cirrotically altered rat liver: in hepatocytes of the second group of rats the total protein content and ploidy levels were higher than those in the first group by 4.7 and 11.5%, respectively.
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PMID:[Effect of "vilon" on cirrhotically changed rat liver. Liver regeneration, and status of glycogen-forming function of hepatocytes]. 1103 62

Effects of acute inhibition of glucose-6-phosphatase activity by the chlorogenic acid derivative S4048 on hepatic carbohydrate fluxes were examined in isolated rat hepatocytes and in vivo in rats. Fluxes were calculated using tracer dilution techniques and mass isotopomer distribution analysis in plasma glucose and urinary paracetamol-glucuronide after infusion of [U-(13)C]glucose, [2-(13)C]glycerol, [1-(2)H]galactose, and paracetamol. In hepatocytes, glucose-6-phosphate (Glc-6-P) content, net glycogen synthesis, and lactate production from glucose and dihydroxyacetone increased strongly in the presence of S4048 (10 microm). In livers of S4048-treated rats (0.5 mg kg(-1)min(-)); 8 h) Glc-6-P content increased strongly (+440%), and massive glycogen accumulation (+1260%) was observed in periportal areas. Total glucose production was diminished by 50%. The gluconeogenic flux to Glc-6-P was unaffected (i.e. 33.3 +/- 2.0 versus 33.2 +/- 2.9 micromol kg(-1)min(-1)in control and S4048-treated rats, respectively). Newly synthesized Glc-6-P was redistributed from glucose production (62 +/- 1 versus 38 +/- 1%; p < 0.001) to glycogen synthesis (35 +/- 5% versus 65 +/- 5%; p < 0.005) by S4048. This was associated with a strong inhibition (-82%) of the flux through glucokinase and an increase (+83%) of the flux through glycogen synthase, while the flux through glycogen phosphorylase remained unaffected. In livers from S4048-treated rats, mRNA levels of genes encoding Glc-6-P hydrolase (approximately 9-fold), Glc-6-P translocase (approximately 4-fold), glycogen synthase (approximately 7-fold) and L-type pyruvate kinase (approximately 4-fold) were increased, whereas glucokinase expression was almost abolished. In accordance with unaltered gluconeogenic flux, expression of the gene encoding phosphoenolpyruvate carboxykinase was unaffected in the S4048-treated rats. Thus, acute inhibition of glucose-6-phosphatase activity by S4048 elicited 1) a repartitioning of newly synthesized Glc-6-P from glucose production into glycogen synthesis without affecting the gluconeogenic flux to Glc-6-P and 2) a cellular response aimed at maintaining cellular Glc-6-P homeostasis.
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PMID:Acute inhibition of hepatic glucose-6-phosphatase does not affect gluconeogenesis but directs gluconeogenic flux toward glycogen in fasted rats. A pharmacological study with the chlorogenic acid derivative S4048. 1134 46

Using cytofluorimetric and biochemical studies on serial supravital liver punctate biopsies, effects of chorionic gonadotropin (CG) on recovery of hepatocyte glycogen-forming function in the cirrhotically altered rat liver were analyzed. The biopsies were taken first from rats with experimental cirrhosis produced by their 6-month-long poisoning with the hepatotoxic poison CCl4, then from the same animals in 1, 3, and 6 month after cessation of their poisoning, either on treatment with CG or with no treatment. In smears of isolated hepatocytes, the contents of the total glycogen (TG) and of its labile and stable fractions (LF and SF, respectively) were measured. In liver homogenates, activities of glucose-6-phosphatase (G6Pase), glycogen phosphorylase, and glycogen synthetase were determined. It was found that the threefold increased TG content in hepatocytes of cirrhotic liver returned to the normal level in 3 months without treatment, while as soon as in 1 month in the case of the treatment with CG. The CG treatment for 3 months resulted in normalization of the glycogen fraction composition that had been changed in cirrhotic liver, whereas without treatment, the glycogen LF/SF ratio remained changed even after 6 months after cessation of the poisoning with CCl4. Activity of G6Pase was fourfold reduced in cirrhosis; in 3 months after the end of poisoning, under effect of CG, the activity increased to the normal level, but somewhat decreased subsequently. In the animals that were not treated with CG, the decrease in the G6Pase activity after the cessation of the CCl4 poisoning was even more marked than in the CG-treated rats. Activities of two other enzymes of glycogen metabolism did not differ statistically significantly from the norm throughout the entire experiment. The data obtained indicate that the use of CG for rehabilitation of the glycogen-forming function of the cirrhotically altered liver is more efficient than other ways of treatment studied previously, such as partial hepatectomy or a high-carbohydrate diet.
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PMID:Glycogen-forming function of hepatocytes in cirrhotically altered rat liver after treatment with chorionic gonadotropin. 1137 Jul 34


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