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)

Studies have been made on glycogen content as well as on the activity of phosphorylase and glucose-6-phosphatase in fast and slow muscles from representatives of 6 classes of vertebrates (Lampetra fluviatilis, Cyprinus carpio, Rana temporaria, Rana ridibunda, Emys orbicularis, hen, rat). Glycogen level and glucose-6-phosphatase activity are either higher in slow muscles, or practically identical in both types of muscles (glucose-6-phosphatase is absent from the fast muscles of hens and rats). On the contrary, phosphorylase activity is higher in fast muscles, this finding being true only for higher vertebrates and lampreys.
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PMID:[Glycogen content and activities of phosphorylase and glucose-6-phosphatase in the fast and slow muscles of representatives of different classes of vertebrates]. 624 64

Glycogen content and glucose-6-phosphatase activity were determined in the both proximal and distal parts of the ligatured ischiadicus nerve of the frog. The results show that endogenous glycogen stores (or derived from them glucose) can move along the nerve and can be utilised in ischiadicus nerve metabolism. These data support our earlier findings that glycogen biosynthesis depends on glucose-6-phosphatase activity.
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PMID:[Glycogen content and glucose-6-phosphatase activity in the ligated frog ischiatic nerve]. 627 Sep 33

The effects of infection with plerocercoids of Spirometra mansonoides on tissue glycogen deposition of rats was determined. Hypophysectomized rats infected for two days had higher liver glycogen concentrations than controls and this effect was greatest after one week. Elevated liver glycogen associated with plerocercoid infection was observed in fed animals both at the beginning and at the end of the light period as well as after an overnight fast. Glycogen phosphorylase (1,4 alpha D glucan: orthophosphate alpha glucosyltransferase EC 2.4.1.1.) was inhibited but glucose-6-phosphatase (EC 3.1.3.9) was unaffected in the livers of infected hypophysectomized rats. While this effect is similar to actions of both growth hormone and insulin, plerocercoid infection had no influence on glycogen of cardiac or skeletal muscle at any time. Plerocercoid infection had no effect on the glycogen concentration of any tissue of intact rats.
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PMID:Spirometra mansonoides: effects of plerocercoid infection on glycogen deposition in rats. 630 Feb 17

The amount and distribution of glycogen as well as the activity of glucose-6-phosphatase (G-6-Pase) in the livers of rats were analyzed by biochemical and/or histochemical techniques. During the first 5 hr of the light cycle, livers of rats were sampled prior to and 30 min following an injection of compound 48/80 or Ringer's solution. Glycogen decreased significantly in response to sampling; however, treatment with compound 48/80 provoked an additional significant decrease in hepatic glycogen. These differences occurred irrespective of the time during the 5 hr that this was studied. The livers of the majority of the rats treated with compound 48/80 displayed a periportal distribution of glycogen, while those treated with Ringer's showed a more uniform pattern. Hepatic G-6-Pase activity was unchanged in either the Ringer's or compound 48/80 treated rats. These results indicated that (1) the significant glycogenolytic response occurs independently of the amount of glycogen present, (2) G-6-Pase activity is not affected within 30 min following the stimulation of glycogenolysis, (3) variation in glycogen patterns during depletion depends on the nature of the stimulus and/or degree of response, and (4) the amount of glycogen available for release is limited.
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PMID:Effects of compound 48/80 on hepatic glycogen and glucose-6-phosphatase early in the diurnal cycle of the rat. 632 66

Glycogen storage diseases (GSD) are inborn errors of glycogen metabolism. Of the eight human GSD types in which the enzymatic deficiency has been identified, spontaneous animal counterparts have been reported for GSD I (glucose-6-phosphatase deficiency) in the mouse, for GSD II (acid alpha-glucosidase deficiency) in the dog, in cattle and in the quail, for GSD III (debrancher enzyme deficiency) in the dog and for GSD VIII (phosphorylase kinase deficiency) in the rat and the mouse. Experimentally induced GSD-like conditions have been described in the rat (Acarbose-induced GSD II-like conditions, iodoacetate-induced symptoms of myophosphorylase (GSD V) and myophosphofructokinase (GSD VII) deficiency) and the chicken (ochratoxin A-induced symptoms of cyclic AMP-dependent protein kinase deficiency). Enzymatic defects that are typical of the human GSD types have not been clearly identified in the induced animal conditions. The homology of animal and human GSD types is discussed. It is concluded that clinical, pathogenic and therapeutic studies of GSD may benefit from the use of animal models. For genetic studies of human GSD these models may prove to be of limited value, as the picture of several human GSD types is already obscured by genetic heterogeneity.
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PMID:Glycogen storage diseases in animals and their potential value as models of human disease. 640 5

The probable involvement of hepatic carbamyl-P in the reciprocal relationship between hepatic ureagenesis and glycogenesis from glucose was explored. Isolated perfused liver preparations from 48-h fasted rats were employed. Moderate (9.2 mM) and relatively high levels of glucose (34 mM) were perfused. Hepatic glycogenesis, glucose-6-P, carbamyl-P, and citrulline levels, hepatic urea formation, and ureagenesis based upon perfusate urea levels were measured. Experimental probes selected to modify hepatic ureagenesis and carbamyl-P production and utilization included: (a) NH4Cl, maintained at 5 mM by continuous infusion (NH4+ is a substrate for carbamyl-P synthase I and glutamate dehydrogenase); (b) norvaline, an inhibitor of ornithine transcarbamylase which catalyzes the first committed step in the urea cycle; and (c) ethoxyzolamide, an inhibitor of carbonic anhydrase which produces HCO3-, an essential substrate for carbamyl-P synthase I. NH4+ increased ureagenesis and decreased glycogenesis. The inclusion of norvaline with NH4+ decreased ureagenesis and increased glycogenesis. Ethoxyzolamide with or without NH4+ inhibited both ureagenesis and glycogenesis, and decreased the hepatic glucose-6-P level. Glycogenesis was greater at 34 mM than 9.2 mM glucose, increased in norvaline-containing preparations correlative with increased availability of carbamyl-P, and decreased when carbamyl-P formation was inhibited by ethoxyzolamide. Kinetic analysis indicated a Km, Glc of 31 mM for glucose phosphorylation preliminary to glycogenesis. Glycogen formation via the "indirect pathway" (i.e. involving extrahepatic glycolysis, transport of lactate to the liver, and glyconeogenesis therefrom) was quantitatively insufficient to account for the observed glycogenesis. Glucokinase is contraindicated by the inverse relationship between hepatic glycogenesis and ATP availability in the ethoxyzolamide-treated preparations. In contrast, carbamyl-P:glucose phosphotransferase activity of the glucose-6-phosphatase system has the characteristics to bridge hepatic ureagenesis and glycogenesis.
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PMID:Glycogenesis from glucose and ureagenesis in isolated perfused rat livers. Influence of ammonium ion, norvaline, and ethoxyzolamide. 813 5

Deficiency of the enzyme glucose-6-phosphatase is the biochemical defect in glycogen storage disease type I (GSD I). Normally this enzyme is present in the liver, intestine and kidneys. The lack of the enzyme in the kidney makes it obvious that glycogen storage will not be restricted to the liver but that also the kidneys will be involved, possibly resulting in renal damage. Glycogen storage in the kidney is most outspoken present in the proximal tubular cells. In case of insufficient metabolic control, a Fanconi-like syndrome can develop, disappearing with improved therapy. Although renal disease has not been considered a problem in GSD I, recent findings indicate that especially in adult patients chronic renal disease is a common complication. In the past gout nephropathy and renal stones were the complications mentioned. Recently it appears that in a considerable number of patients after a period of 'silent' hyperfiltration, renal damage develops with proteinuria, hypertension and renal dysfunction later on. In biopsies of such patients focal glomerulosclerosis is found.
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PMID:Renal complications in glycogen storage disease type I. 831 28

Glycogen synthesis in isolated perfused livers or livers of anesthesized rats (in situ), was studied using radioactively labelled fructose, lactate, and inositol as substrates. The specific radioactivity of glucose and glycogen was measured at various times and compared with that of some intermediates. The results suggest that liver glycogen is formed from the pool of free glucose which in turn is fed by the so-called "direct and indirect pathway" of glycogen synthesis. This points to an important role of glucose-6-phosphatase, an enzyme complex subject to regulation by glucocorticoids, well known promoters of hepatic glycogen synthesis.
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PMID:Glycogen synthesis in rat liver from a pool of free glucose. 847 Nov 3

In an attempt to explain the previous observation of the rise and subsequent fall in glycogen content of the rat visceral yolk sac during the latter half of gestation, the activities of glycogen phosphorylase, glucose-6-phosphatase and lysosomal alpha-glucosidase were measured. Glycogen phosphorylase was found to be present in the yolk sac and, as in adult rat liver, was predominantly in the 'a' (active) form. The specific activity of the enzyme was lower than in adult rat liver, when expressed per mg tissue protein or per mg tissue wet weight, but similar when expressed per mg tissue glycogen. Phosphorylase activity in yolk sac was similar at 16.5 and 18.5 days of gestation. Glucose-6-phosphatase activity was not detectable in the yolk sac at either 15.5 or 18.5 days of gestation. Two lysosomal enzymes, acid alpha-glucosidase and N-acetyl-beta-hexosaminidase, were shown to be present in the yolk sac at higher specific activity than in adult liver. Alpha-Glucosidase activity in yolk sac was similar at 15.5 and 18.5 days of gestation. It is concluded that the net degradation of yolk sac glycogen initiated around 18.5 days of gestation does not serve to provide glucose for the fetus, and may indicate an increased demand for metabolic energy within the yolk sac itself.
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PMID:Glycogen metabolism in the rat visceral yolk sac. 2. Activity of glycogen-degrading enzymes. 871 Aug 2

Mouse renal cell tumors (RCT) were induced in male CBA male mice by 5 subcutaneous injections of 8 mg 1,2-dimethylhydrazine (DMH) per kg body weight once a week. After a lag period of two years the kidneys were removed, and serial cryostat sections of the kidneys were histochemically analyzed for the following parameters: Glycogen content, basophilia, and activities of glycogen synthase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), glucose-6-phosphate dehydrogenase (G6PDH), hexokinase (HK), pyruvate kinase (PK), lactate dehydrogenase (LDH), malic enzyme (ME), succinate dehydrogenase (SDH), alkaline phosphatase (ALPase) and glutamyl-transpeptidase (GGT). RCT displayed the same histochemical profile irrespective of their size and growth pattern. In comparison with normal kidney epithelium, the neoplastic cells exhibited elevated activities of enzymes for glycolysis (HK, PK LDH) and the pentose phosphate pathway (G6PDH) while negative G6Pase and low SDH activity were observed in these cells. The majority of RCT showed high PHO activity and weak staining for SYN. Activities of ALPase and GGT were negative in most of the RCT. Giant cells were detected in some large RCT. Higher activities of glycolytic and mitochondrial enzymes and G6PDH were found in giant cells compared with other tumor cells. Tubular preneoplastic lesions were similar to neoplastic lesions in morphological and histochemical characteristics. The present study revealed that a markedly elevated capacity for glycolysis and the pentose phosphate pathway occurred in renal cell tumors in mice. A similar histochemical pattern in the few preneoplastic tubular lesions observed suggests that these metabolic aberrations emerge early in carcinogenesis, but studies on earlier stages of renal carcinogenesis are needed to substantiate this assumption.
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PMID:[Enzymic spectrum of preneoplastic and neoplastic changes induced by 1,2-dimethylhydrazine in mouse kidneys]. 874 89


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