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:2.7.1.1 (hexokinase)
5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe an enzyme histochemical multistep technique for the demonstration of pyruvate kinase activity. In this technique, a semipermeable membrane is interposed between the incubation medium and the tissue sections, thus preventing diffusion of the enzyme into the medium during the incubation period. In this histochemical system, phosphoenolpyruvate (PEP) donates its phosphate group to ADP in a reaction catalysed by pyruvate kinase. Next, exogenous and endogenous hexokinase catalyses the reaction between ATP and D-glucose to yield D-glucose-6-phosphate and ADP. The D-glucose-6-phosphate is oxidized by exogenous and endogenous D-glucose-6-phosphate dehydrogenase, and concomitantly, the generated electrons are transported via NADP+, phenazine methosulphate and menadione to nitro-BT, which is finally precipitated as formazan. Sodium azide and amytal are included to block electron transfer to cytochromes. The method proved to be of value for the qualitative demonstration of pyruvate kinase activity in tissue sections of kidneys, heart muscle and skeletal muscle. For quantitative studies and for investigating the activity of this enzyme in liver sections, the method cannot be recommended.
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PMID:Histochemical technique for the demonstration of pyruvate kinase activity. 336 51

D-glucose increases O2 uptake by cerebellum mitochondria. This effect is abolished by D-glucose-6-phosphate and D-mannoheptulose. It is proposed that the phosphorylation of D-glucose as catalyzed by bound hexokinase directly affects mitochondrial respiration.
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PMID:Stimulation by D-glucose of mitochondrial respiration. 339 58

Treatment with malathion resulted in an increase in the level of blood glucose and lactate and reduced cerebral glycogen, 2 hr after its administration. The blood pyruvate level was not changed. The activities of glycogenolytic enzymes (glycogen phosphorylase and phosphoglucomutase) were increased significantly in the brain, whereas that of glucose-6-phosphatase remained unchanged. The activity of the glycolytic enzyme-hexokinase was increased significantly in malathion-treated animals, whereas those of the glucose-6-phosphate and lactate dehydrogenases were not significantly changed. The changes in enzyme activities may be a compensatory mechanism to provide energy in the form of glucose to cerebral tissue on account of stimulatory effects in malathion-treated animals.
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PMID:Cerebral glycogenolysis and glycolysis in malathion-treated hyperglycaemic animals. 357 75

Cultured neuroblastoma cells (clone neuro-2a) were used to demonstrate the influence of an anesthetic on energy metabolism by acting on the intracellular distribution of hexokinase activity. First of all, there was to be shown that a relationship between the intracellular hexokinase distribution and energy metabolism actually exists in neuroblastoma cells. Since glucose-6-phosphate could be assumed to be the main regulator of this enzyme distribution, experimental conditions were chosen where the glucose-6-phosphate level was changed significantly. A decrease in the glucose-6-phosphate level in the cells was achieved by deprivation of glucose and oxygen for 30 min. Under these conditions the glucose-6-phosphate level and the soluble hexokinase activity decreased significantly. The effect was reversible when glucose and oxygen were again added to the incubation medium of the cells. On the other hand, the antimetabolite 6-aminonicotinamide produced an accumulation of glucose-6-phosphate which caused an increase in the soluble hexokinase activity. These results brought evidence for a correlation of intracellular hexokinase distribution and energy metabolism. When alpha-(+/-)-5-allyl-1-methyl-5-(1-methyl-2-pentinyl) barbituric acid (methohexital) was added to the incubation medium of the neuroblastoma cells, a dose-dependent increase in soluble hexokinase activity was measurable, whereas the glucose-6-phosphate level was decreased at least within a therapeutically relevant dosage range of the anesthetic. This effect was reversible when methohexital was washed out from the cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of methohexital on the relationship between hexokinase distribution and energy metabolism in neuroblastoma cells. 359 43

We studied the effect of spontaneous long-term (9-10 months) diabetes on the heart of Chinese hamsters (CHAD strain) to elucidate the relationship between diabetes mellitus and cardiomyopathy. The diabetic hamsters, aged approximately 11 months, showed body weight loss, hyperglycemia (mean fasting plasma glucose 402 mg/dl), hypoinsulinemia, hyperlipidemia and ketonemia. The diabetic hamsters showed reduced activities of cytoplasmic glycolytic key enzymes; hexokinase, pyruvate kinase and phosphofructokinase, increases in cardiac glycogen and glucose-6-phosphate contents and a 40% decrease in cardiac ATP content, indicating decreased energy production. An accumulation of myocardial triglyceride and cholesterol was found in the diabetic hamsters. In addition, the cardiac norepinephrine content was increased in the diabetic hamsters, suggesting the presence of autonomic nervous disorder. Increased heart weight and thickening of the septum and both ventricular walls were found in the diabetic hamsters. Light-microscopic analysis revealed that 42.9% of the diabetic hamsters had myocardial degeneration without any vascular lesion of extramural large and intramural small vessels, whereas the non-diabetic controls had no myocardial or vascular lesions. These data suggest that the diabetic Chinese hamsters had cardiomyopathy, which is possibly caused by extravascular factors such as metabolic or autonomic nervous disorder although conclusive evidence is lacking.
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PMID:Metabolic and morphological changes of the heart in Chinese hamsters (CHAD strain) with spontaneous long-term diabetes. 366 31

Leg glucose uptake (LGU) during submaximal (50% maximal O2 uptake) and maximal dynamic exercise (97%) has been quantified from the product of the leg blood flow and the arterial minus femoral venous glucose concentration. Muscle biopsies were also obtained. During 15 min of submaximal exercise the mean LGU values ranged from 1.07 to 1.25 mmol/min, which demonstrates that LGU was stable under this condition. In contrast, during maximal exercise LGU increased continuously, reaching 2.38 +/- 0.22, 2.95 +/- 0.32, and 3.82 +/- 0.34 mmol/min after 2, 4, and 5.2 min (fatigue), respectively. The mean LGU was negatively related to the mean muscle phosphocreatine content (r = -1.00;P less than 0.01). Intracellular glucose-6-phosphate (G-6-P) and glucose were very low at rest and did not change significantly during submaximal exercise (P greater than 0.05). However, at fatigue G-6-P and glucose increased substantially and were both 8.5 mmol/kg dry muscle (P less than 0.001). These findings demonstrate that during heavy exercise glucose accumulates in the cell probably due to hexokinase inhibition by G-6-P, and thus the rate of glucose utilization appears to be lower than the rate of glucose uptake. It is suggested that 1) LGU during short-term exercise is dependent on the energy state of the muscle and 2) LGU is equal to leg glucose utilization during submaximal exercise but is in excess of utilization during heavy exercise.
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PMID:Leg glucose uptake during maximal dynamic exercise in humans. 372 65

It was found that in the presence of Mg2+ (pH 7.5) rat skeletal muscle hexokinase isozyme II is firmly adsorbed on mitochondrial and artificial phospholipid membranes (lecithin liposomes). In both cases the adsorption isotherm has similar quantitative and qualitative characteristics, which points to the absence of specific binding sites on the membranes. Under these conditions, immobilization of hexokinase on various membranes is concomitant with similar changes in the enzyme stability upon storage as well as with the pH-dependence of the enzyme activity. It was demonstrated that the bound hexokinase form has a greater value of V, an increased affinity for glucose and a decreased sensitivity to the inhibitory action of glucose-6-phosphate as compared to the free form. Besides, this form is in a greater degree subjected to the inhibitory influence of ADP with respect to glucose. In this case, the enzyme affinity for ATP and the Ki value for ADP with respect to ATP is practically the same both for the free and membrane-bound forms. The data obtained suggest that the phospholipid component of mitochondrial membranes participates in the enzyme binding in the presence of Mg2+. It was assumed that the model system used in the present study, i.e., hexokinase-Mg2+-liposomes, may be successfully used for the analysis of an adsorption mechanism of regulation of hexokinase activity in the cell.
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PMID:[Interaction of hexokinase II isoenzyme from rat skeletal muscles with lecithin liposomes]. 373 Apr 44

The notion of the "primary block" of cellular metabolism designated as "metabolic system" is introduced. Metabolic system is defined as a metabolic pathway which corresponds to the structurally ordered multienzyme complex. The complex of glycolytic enzymes which catalyzes the anaerobic reduction of glucose-6-phosphate with production of ATP may serve as an example of metabolic system (this complex does not contain hexokinase). The complex is formed on thin filaments of I-band of the muscle fibres or on the dimers of band 3 protein embedded in the erythrocyte membrane. The fixation of the multienzyme complex to the support of the biological nature provides the material basis for regulation of the metabolic system by chemical signals produced by the higher levels of metabolic control. Owing to interaction with anchor protein of the support the chemical signals exert the general control of functioning of the multienzyme complex (switching on-switching off the metabolic system). It is assumed that glycolytic system in skeletal muscles is stimulated by Ca2+ ions which interact with the anchor protein of the support (troponin C).
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PMID:The role of multienzyme complexes in integration of cellular metabolism. 374 56

Enzymes of the Embden-Meyerhof-Parnas pathway and hexose monophosphate shunt were examined in cytoplasmic extracts of three serovars of Ureaplasma urealyticum. We found no glucose-6-phosphate or 6-phosphogluconate dehydrogenase, hexokinase, phosphoglucose isomerase, aldolase, or lactic dehydrogenase activities. We failed to find cytochrome pigments in extracts and found no significant production of 14CO2 from [U-14C]glucose, nor did we find oxygen-dependent reduced nicotinamide adenine dinucleotide oxidase activity. Lactic acid was found only at trace levels in spent culture fluids. Ureaplasmas are apparently nonfermentative and are unlike all other mollicutes in that they have no detectable oxygen-dependent reduced nicotinamide adenine dinucleotide oxidase activity.
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PMID:Metabolic distinctiveness of ureaplasmas. 379 29

It is shown in experiments on rats that the early postischemic period after 1- and 1.5-hour ischemia of kidneys is characterized by a decrease in the damage of the glycolytic system site which induces glucose-6-phosphate transformation into lactate and by an increase in the inhibition intensity of the initial hexokinase reaction of glycolysis. In the postischemic period after more prolonged (2-, 3-hour) ischemia the damage of the glycolytic system develops also at the site of glucose-6-phosphate transformation into lactate. Administration either of the nucleotide complex (NAD and AMP) or calmodulin inhibitors (aminazine and zinc sulphate) to rats prior to two-hour occlusion of kidneys vessels promotes a decrease in the inhibition of the glycolytic system activity in the postischemic period. At the same time the separate and combined application of zinc sulphate and triftazin (the most intensive calmodulin inhibitor) is not efficient. The positive effect of NAD, AMP and aminazine on the state of the glycolytic kidney system in the postischemic period correlates with the improvement of the blood microcirculation processes in them.
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PMID:[Glycolysis in the rat kidney shortly after ischemia and administration of calmodulin inhibitors, AMP and NAD]. 379 79


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