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)

1. Two experiments were performed to examine the effects of duodenal glucose infusion on hepatic enzyme activities in sheep. 2. Glucose infusion significantly increased the specific activities of phosphofructokinase, pyruvate kinase and 6-phosphogluconate dehydrogenase and significantly reduced the specific activity of glucose-6-phosphatase suggesting that the pathways of glucose breakdown are increased, and gluconeogenesis decreased, in glucose-infused animals. 3. The results are discussed in relation to the effects of diet on liver metabolism in sheep.
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PMID:The effects of duodenal glucose infusion on some hepatic enzyme activities in sheep. 710 53

The influence of fructose feeding for 1 to 12 days on the activity of enzymes of glycolysis and gluconeogenesis was studied in the jejunal mucosa and the liver of rats. In the jejunal mucosa fructose feeding leads to an increase in the activity of 6-phosphofructokinase (p less than 0.05) and fructose-1.6-bisphosphate aldolase (p less than 0.05), while the activity of hexokinase and glucose-6-phosphate dehydrogenase remains unchanged. Fructose feeding increases the activity of fructose-bisphosphatase in the jejunal mucosa, however, the absolute values of this enzyme remain low (less than 10%) when compared to those in the liver. In the liver fructose feeding is followed by a marked increase of the activity of fructose-bisphosphatase and glucose-6-phosphate dehydrogenase. In contrast, the activity of glucose-6-phosphatase decreases significantly under a fructose enriched diet. The enzyme activity rose to a maximum within 3 days; in the following time of observation no major changes occurred. The results are in accordance with the assumption that fructose feeding leads in the jejunal mucosa mainly to adaptive alterations of the activity of those enzymes which are involved in the breaking-down of fructose, whereas in the liver the activity of those enzymes is increased, which take part in the new synthesis of glucose-6-phosphate or which direct glucose-6-phosphate into the pentose-phosphate.
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PMID:Effect of fructose feeding on the activity of enzymes of glycolysis, gluconeogenesis, and the pentose phosphate shunt in the liver and jejunal mucosa of rats. 727 91

Existing models for glycolytic oscillations are not based on detailed experimental kinetics of the glycolytic enzymes. Here, a model is constructed to fit the kinetics of skeletal muscle phosphofructokinase with respect to variations in AMP, ATP, fructose-6-P, and fructose 1,6-P2 levels. A Monod-Wyman-Changeux model for a tetrameric enzyme is considered. However, it is found that the kinetic data fit considerably better with an assumption of identical, independent subunits. With parameters that fit these data and with a previous model for the rest of glycolysis, product activation of phosphofructokinase leads to oscillations of glycolytic intermediates and [ATP] resembling those observed experimentally in muscle extracts. The period is several minutes. The model can also produce oscillations at neutral pH and with [ATP] representative of an intact cell. Under both conditions the mean concentrations and oscillations vary with the rate of glucose phosphorylation in a plausible manner only if some amount of glucose-6-phosphatase or glucose-6-P dehydrogenase activity is assumed or if hexokinase is inhibited by glucose-6-P. Also, the model can be reduced to two variables for ease of analysis and the oscillation mechanism thereby illustrated.
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PMID:A model for glycolytic oscillations based on skeletal muscle phosphofructokinase kinetics. 764 10

A 12-wk feeding trial was conducted to study the influence of chromic oxide (Cr2O3) on carbohydrate utilization and digestibility by tilapia, Oreochromis niloticus x O. aureus. Two levels of chromic oxide (0.5 and 2%) were each incorporated into diets containing glucose or starch. Chromic oxide was added at 0 or 8 wk. The diets were fed to triplicate groups of fish weighing 1.11 +/- 0.05 g. Fish fed the starch diet had greater (P < 0.05) weight gain, feed efficiency ratio, protein efficiency ratio, protein deposition and digestibility of protein, lipid, carbohydrate and dry matter than fish fed the glucose diet irrespective of the time and level of chromic oxide supplementation. Fish fed the glucose diet with 0.5% chromic oxide had higher weight gain, feed efficiency ratio, protein efficiency ratio and protein deposition than fish fed the glucose diet with 2% chromic oxide. The ingredient digestibility estimated using 0.5% chromic oxide as the marker was greater than that estimated with 2% chromic oxide. Higher phosphofructokinase and lower glucose-6-phosphatase activity was found in fish fed the starch diet than in fish fed the glucose diet regardless of the time and level of chromic oxide inclusion. Fish fed the glucose diet with 0.5% chromic oxide had higher phosphofructokinase activity and lower tissue chromium concentration than fish fed the glucose diet with 2% chromic oxide irrespective of chromic oxide inclusion time. These data suggest that the level of chromic oxide in the diet alters glucose utilization by tilapia and affects nutrient digestibility by tilapia. The time of chromic oxide inclusion had no effect on carbohydrate utilization and digestibility.
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PMID:Carbohydrate utilization and digestibility by tilapia, Oreochromis niloticus x O. aureus, are affected by chromic oxide inclusion in the diet. 772 2

To quantitatively test the theory that glucokinase controls the rate of glucose metabolism and therefore the rate of insulin secretion, a minimal mathematical model of glycolysis in the pancreatic beta-cell was developed. The model represents our current hypothesis of how the normal beta-cell transduces the glucose signal. In this report, the model was used to address questions regarding the control strength of transport, hexokinase, glucose-6-phosphatase, and phosphofructokinase in the metabolism of glucose. The hypothesis that fructose 6-phosphate and a protein regulator modulate glucokinase activity was evaluated by simulation analysis, as was the possibility that glucose-6-phosphatase, working in concert with phosphofructokinase, can modulate the glucose-sensing system. It was found that, in the absence of glucose-6-phosphatase, transport, hexokinase, and phosphofructokinase do not greatly influence the rate of glucose metabolism unless their activities are dramatically altered from the measured values. Glucose metabolism was profoundly affected by the activity of glucokinase. However, in the presence of glucose-6-phosphatase, the ratio of glucose-6-phosphatase to phosphofructokinase activities was a very important parameter, and this potential control mechanism deserves more attention. The results further support the notion that glucokinase is indeed the glucosensor of the beta-cell and that modeling the system in toto provides quantitative evaluation needed to interpret the experimental tests of hypotheses.
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PMID:Mathematical model of beta-cell glucose metabolism and insulin release. I. Glucokinase as glucosensor hypothesis. 773 79

In sporadic Alzheimer's disease (AD), a number of metabolic alterations to the brain have been observed soon after the onset of the initial clinical symptoms. In particular, impairments of glucose utilization and related metabolic pathways are prominent and well-established findings in incipient AD, resembling metabolic abnormalities such as have been found in noninsulin-dependent diabetes mellitus. To mimic these abnormalities, we administered an intracerebroventricular (icv) injection of streptozotocin (STZ) to rats and studied the effects of glucose and glycogen metabolism in the cerebral cortex and hippocampus compared with controls. The enzymatic activities studied dropped significantly by 10-30% in brain cortex (cort.) and hippocampus (hc) 3 and 6 weeks after icv STZ injection: hexokinase (15% 3 weeks cort.; 14% 6 weeks cort.; 12% 3 weeks hc; 28% 6 weeks hc), phosphofructokinase (15%; 15%; 24%; 15%), glyceraldehyde-3-phosphate dehydrogenase (10%; 12%; 30%; 19%), pyruvate kinase (22%; 13%; 22%; 28%), glucose-6-phosphatase (10%; 23%; 14%; 19%) and phosphorylase a (22%; 11%; 30%; 15%). The content of glycogen was significantly higher in STZ-treated rats than in control animals (7% 3 weeks and 15% 6 weeks in cortex). In contrast to the reduced enzymatic activities, we observed no changes in the concentrations of the glycolytic intermediates glucose, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, pyruvate, lactate and glucose-1-phosphate. These data clearly indicate reduced glycolytic enzyme activity after icv administration of STZ and suggest gluconeogenesis consequent on abnormalities in glucose breakdown. This model may thus be assumed to be a useful tool to investigate pathogenetic factors involved in sporadic dementia of Alzheimer type.
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PMID:Action of the diabetogenic drug streptozotocin on glycolytic and glycogenolytic metabolism in adult rat brain cortex and hippocampus. 823 64

We studied the effect of selenium on the glycolysis and gluconeogenesis system in the rat liver. Significant decreases in glucose level in the serum were observed from the 4th day after daily intraperitoneal (i.p.) administration of selenite (173 micrograms/kg, 78.9 micrograms/kg of selenium base equivalent). Selenium was also effective in reducing a precursor of gluconeogenesis, lactate, alanine or glycerol, in the serum. Moreover, there were significant decreases in the activities of pyruvate carboxylase and glucose-6-phosphatase, a rate-limiting enzyme of gluconeogenesis, in the liver of selenium-treated rates. On the contrary, the activities of glycokinase and phosphofructokinase, a rate-limiting enzyme of glycolysis, in the liver of rat treated with selenium significantly increased in comparison with the control group. These data, therefore, indicated that the hypoglycemic effect of selenium might be due to the acceleration of glucose metabolism and the inhibition of glucose synthesis in the liver, suggesting a decrease in a source of precursor supply for the gluconeogenesis.
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PMID:[Effects of selenium on the glycolysis and gluconeogenesis system in rat liver]. 836 30

Expression of key regulatory enzymes involved in glucose metabolism was studied in the livers of Otsuka Long-Evans Tokushima fatty (OLETF) rats, a model of non-insulin dependent diabetes mellitus. The activity and mRNA levels of glucokinase and L-type pyruvate kinase was increased in the liver of OLETF rats compared with control rats. There was no such remarkable change in liver-type phosphofructokinase. The activities of glucose-6-phosphatase and fructose-1,6-biphosphatase also increase despite high plasma levels of glucose and insulin. The activity of phosphoenolpyruvate carboxykinase did not show any significant change. The mRNA levels for fructose-1,6-biphosphatase, and phosphoenolpyruvate carboxykinase exhibited no marked changes. These results suggest that the expression of glucose-6-phosphatase and fructose-1,6-biphosphatase is disordered in OLETF rats.
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PMID:Disordered expression of hepatic glycolytic and gluconeogenic enzymes in Otsuka Long-Evans Tokushima fatty rats with spontanteous long-term hyperglycemia. 860 25

The effectiveness of gossypol as an antifertilizing agent is due to the severe injuries or death that this drug produces on spermatozoa and spermatides. Several in vitro and in vivo studies have shown that spermatozoal lactic and malic dehydrogenases are inhibited by gossypol; and that these are more susceptible than the somatic enzymes. Notwithstanding, the in vivo effects on other somatic enzymes have been poorly analyzed. The present study shows that gossypol did not produce toxic effects on eight erythrocytic enzymes of male hamsters that were fed daily with 20 mg of gossypol/kg, for 1, 3, 5 or 10 days. The enzymatic activities analyzed were: adenylate kinase, hexokinase, glucose-6-phosphatase, glucose phosphoisomerase, phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglyceratokinase and pyruvate kinase.
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PMID:Orally administered gossypol has no effect on eight hamster erythrocytic enzymes. 874 2

Crude extracts containing the enzymes obtained from mouse liver were incubated with 3-deoxyglucosone (3-DG), and then subjected to assay of the activities of enzymes responsible for glucose metabolism. Hexokinase and glucose-6-phosphate dehydrogenase activities were decreased by 3-DG and hexokinase activity was strongly inhibited time and concentration dependently, while glucokinase, glucose-6-phosphatase, and phosphofructokinase activities were scarcely affected. These results suggest that 3-DG inhibits the intake of glucose in the liver and a connection with development of diabetes.
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PMID:Effect of 3-deoxyglucosone on the activities of enzymes responsible for glucose metabolism in mouse liver. 887 29


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