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)

The effect of cooling and subsequent rewarming on the tissue respiration of canine hearts was studied during polycomponent ether-oxygen anaesthesia. The tests included the determinations of the activity of the dehydrogenases of the cytrate cycle, the content and activity of chromoproteids, the respiration rate of the mitochondrias on succinate, glutamate and ketoglutarate, the content of glycogen, the activity of the phosphorylases, hexokinase, lactate dehydrogenase, the content of lactate, pyruvate, adenyl nucleotides and creatine phosphate. Significant changes were noted in the content and activity of the above substances, acceleration of mitochondrial respiration, reduced energy regulation of respiration, and decreased amount of the adenyl components. It is suggested that under artificial hypothermia the processes of chromoproteids biosynthesis are enhanced, which results in an increased power of terminal respiration, and conformational rearaangements of the enzymes connected with the membranes occur.
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PMID:[Characteristics of energy metabolism in the myocardium under artificial hypothermia]. 19 79

The purpose of the present investigation was to demonstrate how the intracellular distribution of hexokinase was influenced by anaesthetics. The experiments were carried out using mice in vivo and the isolated perfused rat brain. Thiopentone (100 mg/kg i.p.) produced an increase of soluble hexokinase activity in brains of mice which were removed from the skull in 45 s to 120 s. A solubilization of hexokinase activity was demonstrable in the surgical stage of anaesthesia, when the animals awoke redistribution to control values was measurable. A dose dependent influence of thiopentone on hexokinase distribution was demonstrated in the isolated perfused rat brain. When the thiopentone concentration in the perfusion medium was increased (0.05-0.8 mM) the soluble hexokinase activity was elevated while the EEG activity was reduced up to isoelectricity.
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PMID:[Anaesthesia and intracellular distribution of cerebral hexokinase (author's transl)]. 74 96

The control of hexokinase activity probably is accomplished by regulating the partitioning of the enzyme between soluble and particulate forms, the latter being more active. In the present investigation we have examined the thiopental effect on the cerebral hexokinase distribution. In anesthesia, after administration of thiopental to male Sprague Dawley rats, the increase of the soluble fraction of hexokinase was dose dependent. The change in the intracellular hexokinase distribution was reversible and lasted as long as general anesthesia existed. Also in experiments in vitro a solubilization of the mitochondrial hexokinase by thiopental (0.1--1 mM) occurred; it was depending on drug concentration. An inhibition of hexokinase was found neither in the total brain extract, nor in the soluble or the particulate fraction. The results suggest that phosphorylation of glucose in brain may be suppressed in anesthesia by shifting hexokinase activity from a more active mitochondrial form to its less active soluble form. This effect seems to be caused by a direct action of thiopental and is obviously correlated with anesthesia.
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PMID:Solubilization of brain mitochondrial hexokinase by thiopental. 88 49

We evaluated the effect of sialadenectomy on hexokinase activity and on rates of lactate formation and of [U-14C]glucose decarboxylation in 3 cellular fractions of the small intestine epithelium from male adult mice. The surgery was carried out under ether anesthesia and a sham-operated group was used as control. Three cell fractions were obtained by shaking the inverted small intestine: 1) tip of the villus, 2) villus and 3) villus and crypt cells. Five days after sialadenectomy, hexokinase activity was reduced in fractions 1 (3.53 +/- 0.65 vs 1.98 +/- 0.25 nmol min-1 mg protein-1, expressed as mean +/- SEM for 7 mice) and 3 (5.01 +/- 0.55 vs 3.15 +/- 0.42 nmol min-1 mg protein-1, mean +/- SEM for 7 mice). After removal of the submandibular glands, the rates of lactate formation were decreased in fractions 2 (4.16 +/- 0.54 vs 2.30 +/- 0.25, mean +/- SEM for 10 and 11 mice, respectively) and 3 (1.74 +/- 0.24 vs 0.87 +/- 0.14, mean +/- SEM for 13 mice) and the rates of [U-14C] glucose decarboxylation were reduced in fraction 1 (1.14 +/- 0.12 vs 0.61 +/- 0.10, mean +/- SEM for 11 and 12 mice, respectively). We conclude that the secretion of submandibular glands plays a physiological role in the control of glucose metabolism in enterocytes.
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PMID:Possible role of the submandibular glands in the control of glucose metabolism in mouse enterocytes. 134 44

1. Changes in the content and concentration of glycogen and in the activity of a number of enzymes involved in glucose and glycogen metabolism were studied in the rat hemidiaphragm after unilateral denervation. 2. After nerve section the tissue hypertrophies; this hypertrophy is said to be confined to the smaller red fibres and not to the white. 3. The total hexokinase activity increases, whereas that of total glycogen phosphorylase decreases. The specific activity of phosphorylase a, determined after Halothane anaesthesia, remains fairly constant. 4. In fed animals the denervated tissue stores less glycogen, but in the early stages its glycogen content does not fall on starvation. 5. The effect of denervation on the specific activities of several other characteristically white-fibre enzymes are not consistent with the response of glycogen phosphorylase; the increase in content of glyceraldehyde 3-phosphate dehydrogenase and lactate dehydrogenase is thought to be related to proliferation of the sarcoplasmic reticulum. 6. The ratio of lactate dehydrogenase M/H subunits increases at the height of the hypertrophy, but then declines as the mass of the tissue falls. 7. The chronology of these changes in enzyme activities suggests a multiplicity of distinct responses after nerve section not consistent with any one model, either specific fibre development or reversion to de-differentiated, foetal-type metabolism.
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PMID:Effects of denervation on the glycogen content and on the activities of enzymes of glucose and glycogen metabolism in rat diaphragm muscle. 463 92

The effect of thiopentone, etomidate and flunitrazepam on cerebral energy metabolism was investigated in the male Wistar rat. Brain cortex was deep-frozen in situ under steady state conditions (normotension, normothermia, normoxia and normocapnia) of a standardized anaesthesia. Anaesthesia with thiopentone led to an decrease in glycolytic flux on the level of the hexokinase and/or phosphofructokinase reaction as well as reduced citric acid cycle intermediates. The brain cortex levels of high-energy phosphates however are unchanged thus indicating an adequate supply of energy for the brain. Similar results were obtained when anaesthesia was induced with etomidate and flunitrazepam. In spite of the fact that flunitrazepam seemed not to influence the phosphofructokinase reaction an equivalent hypnotic dose of each drug led to comparable metabolic effects in the brain cortex.
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PMID:[The effects of thiopentone, etomidate and flunitrazepam on cerebral energy metabolism in the rat (author's transl)]. 610 37

It has been demonstrated in previous work that hexokinase is solubilized from the mitochondrial membrane in anesthesia. In the present investigation this effect was strongly correlated with the surgical stage of anesthesia by the application of thiopental to rats (80 mg/kg), mice (100 mg/kg) and guinea pigs (32 mg/kg). The solubilization of hexokinase was demonstrable, too, in different areas of rat brains under thiopental treatment (80 mg/kg). In order to elevate the cerebral concentration of glucose 6-phosphate, which is the most potent substrate for the solubilization of bound hexokinase, male Sprague-Dawley rats were pretreated with the antimetabolite 6-aminonicotinamide (6-AN). After i.p. injection of 6-AN (35 mg/kg) we measured an increased activity of soluble brain hexokinase in the same order of magnitude as it was determined in anesthesia. Thiopental application did not show a further significant increase. A solubilization of hexokinase activity by 6-AN was not measurable in vitro. Furthermore, we examined the other key enzymes in the glycolytic pathway. We found a competitive inhibition of phosphofrucktokinase activity by thiopental, but no inhibition of hexokinase and pyruvate-kinase activity.
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PMID:Key enzymes of glycolysis in brain as influenced by thiopental. 644 16

In thiopental anesthesia of rats cerebral mitochondrial hexokinase activity was solubilized. This solubilization was also observed when the period necessary for the removal of the rat brain was shortened to 15 s by brain blowing. The influence of the drug on the binding of hexokinase activity to mitochondria of brain, liver and neuroblastoma cells was studied in vitro. Solubilization of hexokinase activity was achieved in all systems at therapeutically relevant thiopental concentrations. On the other hand, chlorpromazine as a highly lipophilic drug only solubilized hexokinase activity at concentrations being already lytic to the membrane. Thus, it is concluded that thiopental solubilize hexokinase activity by affecting the mitochondrial membrane, and that this effect is not only dependent on the lipophilic character of a drug.
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PMID:Solubilization of hexokinase activity by an effect of thiopental on the mitochondrial membrane. 707 Nov 27

Mitochondrially bound brain hexokinase is solubilized by anesthetics and this effect has been suggested to contribute to anesthesia. In the present investigation the influence of the metabolic inhibitor 2-deoxy-D-glucose (2-DOG) was studied. An isolated rat brain preparation was used to avoid the contribution of peripheral reactions. Isolated rat brains were perfused for 45 min with media containing 4 mmol/l glucose, 10 mmol/l 2-DOG and/or 0.4 mmol/l thiopental. The EEG was monitored and acetylcholine, 2-DOG and its 6-phosphate, as well as the intracellular distribution of hexokinase activity were determined in brain tissue. Soluble hexokinase activity in brain cortex was enhanced by 2-DOG, as also by thiopental, and even more pronounced by both drugs used together, Results from in vitro experiments suggest that solubilization of mitochondrial hexokinase after 2-DOG is mediated by intracellularly accumulated 2-DOG-6-phosphate. 2-DOG produced a significant impairment of neuronal activity, revealing EEG patterns similar to those caused by thiopental anesthesia. Cortical acetylcholine levels were elevated by 2-DOG, as well as by thiopental, and again both drugs showed an additive effect when used in combination. This effect which may be the result of an inhibition of acetylcholine release, was also detectable in mice in vivo after 5 g 2-DOG/kg i.p., whereas the same dose of 3-O-methylglucose had no effect. The results provide further evidence that mitochondrial hexokinase may be involved in the relationship between cerebral metabolism and brain function.
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PMID:Relationship between brain mitochondrial hexokinase and neuronal function: comparable effects of 2-deoxy-D-glucose and thiopental. 712 20

The purpose of the present investigation was to study the effect of alpha-(+/-)-5-allyl-1-methyl-5-(1-methyl-2-pentinyl) barbituric acid (methohexital, Brevimytal sodium) on brain energy metabolism. The model of the isolated perfused rat brain was used. The high-energy phosphates, some substrates of glycolysis and the intracellular distribution of hexokinase activity were measured in the cortical tissue of the isolated rat brain after 30 min of perfusion, after ischemia or anoxia and after various recovery periods. The EEG was recorded as a parameter of the neuronal activity. The following results were obtained: 1. Ischemia and anoxia accelerated the glycolysis rate which was inhibited by methohexital. 2. The energy metabolism was more rapidly normalized after ischemia or anoxia when methohexital was added to the perfusion medium (0.2 mmol/l). 3. Compared to the corresponding preparation, the spontaneous electrical activity of the isolated brain was maintained in ischemia or anoxia for a longer period and appeared again more rapidly in the recovery periods when methohexital was present. 4. Phosphofructokinase activity was inhibited by methohexital in the recovery period after ischemia or anoxia, respectively. 5. Inhibition of hexokinase activity predominated in the surgical stage of anesthesia when glycolysis rate was not accelerated. Methohexital seemed to inhibit hexokinase activity by solubilizing the mitochondrial bound form.
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PMID:[Mechanisms of the protective effect of methohexital on cerebral energy metabolism]. 720 67


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