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)

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

This short review describes the role of progesterone in the insulin-resistance of pregnancy and the present knowledge of the intracellular mechanisms of action of the steroid in carbohydrate metabolism of female rat adipocytes. Observations concerning steroid effects on the binding of insulin to its specific receptors are often contradictory, and depend on cells used to study it. It is now generally accepted that, in isolated adipocytes, the decreased responsiveness to insulin produced by progesterone is due to a post-receptor effect. Furthermore, basal glucose metabolism (in the absence of insulin) is decreased by progesterone treatment and by the acute effect of progesterone when added directly into the incubation medium. Progesterone induces an intrinsic post-receptor effect which is related to decreased phosphorylation of glucose by hexokinase but has no effect on glucose transport. The effect on hexokinase activity is an indirect one taking place either before or after activation of the enzyme. During the last decade, a large body of evidence (Xenopus oocytes and other cells) indicates that steroids interact with the cell surface rather than penetrating the cell and interacting exclusively with a nuclear receptor. The second messengers, such as cyclic AMP and calcium, play a major role in this non-genomic mechanism. The direct and rapid effect (20 min.) of progesterone in adipocytes supports the non-genomic mechanism of action; there is neither any lag period prior to the appearance of the physiological response nor any inhibition of protein synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carbohydrate metabolism of female rat adipocytes: effects and mechanisms of action of progesterone. 381 56

Inositol 1,4,5-trisphosphate (InsP3) releases Ca2+ from the non-mitochondrial Ca2+ store site of various types of cells. To study the mechanisms of the Ca2+ release from the store site, the effect of InsP3 on the passive Ca2+ release and influx, and the active Ca2+ uptake in the presence of oxalate, was examined using saponin-treated guinea pig peritoneal macrophages. InsP3 stimulated the passive Ca2+ release and influx. Although InsP3 slightly inhibited the active Ca2+ uptake in the presence of oxalate, it seems unlikely that the Ca2+ release by this agent is caused by the inhibition of the Ca2+ uptake, because the addition of apyrase or hexokinase (which removes ATP within 30 s, so that no more Ca2+ can be accumulated) or vanadate (which inhibits the Ca2+ uptake) resulted in very slow release of Ca2+. These results suggest that the Ca2+ permeability of the Ca2+ store membrane is increased by InsP3. InsP3 did not cause an increase in the Ca2+ permeability of phospholipid vesicles (liposomes), indicating that this agent may bring about Ca2+ release by a specific effect on the physiologically relevant Ca2+ channels or carriers in the non-mitochondrial Ca2+ store site. The passive Ca2+ release by InsP3 was enhanced by ATP and an unhydrolyzable ATP analogue, 5'-adenylyimidodiphosphate, but not by ADP or AMP. The passive Ca2+ release by InsP3 was observed even at 0 degree C.
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PMID:Increase in Ca2+ permeability of intracellular Ca2+ store membrane of saponin-treated guinea pig peritoneal macrophages by inositol 1,4,5-trisphosphate. 387 10

The kinetic mechanism of rat skeletal muscle hexokinase (hexokinase II) was investigated in light of a proposal by Cornish-Bowden and his co-workers (Gregoriou, M., Trayer, I. P., and Cornish-Bowden, A. (1983) Eur. J. Biochem. 134, 283-288). These investigators reported that the kinetic mechanism is ordered, with glucose adding before ATP and ADP dissociating from hexokinase before glucose-6-P. In addition, these workers suggest that glucose-6-P and ATP add to allosteric sites on hexokinase. We investigated the mechanism of action of hexokinase II by studying initial rate kinetics in the nonphysiological direction and by isotope exchange at chemical equilibrium. The former experiments were carried out in the absence of inhibitors and then with AMP, which is a competitive inhibitor of ADP, and with glucose 1,6-bisphosphate, a competitive inhibitor of glucose-6-P. The findings from these experiments suggest that the kinetic mechanism is rapid equilibrium Random Bi Bi. Isotope exchange at equilibrium studies also supports the random nature of the muscle hexokinase reaction; however, they also suggest that the mechanism is partially ordered, i.e. there is a preferred pathway associated with the branched mechanism. Approximately two-thirds of the flux through the hexokinase reaction involves the glucose on first glucose-6-P off last branch of the Random Bi Bi mechanism. These results imply that the kinetic mechanism is steady state Random Bi Bi. There is some evidence to suggest that glucose-6-P binds to an allosteric site on muscle hexokinase, but none to suppose that ATP binds allosterically. Analysis of the mechanism of Gregoriou et al. suggests that it is at variance with the findings of this report as well as with data available from other laboratories.
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PMID:Initial rate and isotope exchange studies of rat skeletal muscle hexokinase. 390 69

Muscular glycolytic fuels, intermediates and end-products (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), Krebs cycle intermediates (citrate, alpha-ketoglutarate, succinate, malate), related free amino acids (glutamate, alanine), ammonia, energy store (creatine phosphate), energy mediators (ATP, ADP, AMP) and energy charge potential were evaluated. Furthermore the maximum rate (Vmax) of the following muscular enzyme activities was evaluated in the crude extract and/or mitochondrial fraction: for the anaerobic glycolytic pathway: hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase; for the tricarboxylic acid cycle: citrate synthase, malate dehydrogenase; for the electron transfer chain: total NADH cytochrome c reductase, cytochrome oxidase. The rat gastrocnemius muscles were analyzed in normoxia and after repeated, alternate hypoxic and normoxic exposures (12 hours of hypoxia daily; for 5 days). Naftidrofuryl was administered daily at three different doses: 10, 15 and 22.5 mg/kg i.m., 30 min before the beginning of the experimental hypoxia. The biochemical adaptation to intermittent normobaric hypoxic-normoxic exposures was characterized by the decrease of the muscular contents of creatine phosphate, citrate, alpha-ketoglutarate and glutamate. This adaptation occurred in absence of significant changes in the Vmax of the muscle enzymes tested. By naftidrofuryl treatment, in gastrocnemius muscle from hypoxic rats both alpha-ketoglutarate and creatine phosphate contents maintained normal values, while glutamate concentration remained reduced to subnormal values. With the exception of hexokinase, naftidrofuryl treatment did not modify the Vmax of marker enzymes related to energy transduction.
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PMID:Adaptation of skeletal muscle energy metabolism to repeated hypoxic-normoxic exposures and drug treatment. 401 59

Muscular glycolytic fuels, intermediates and end-products (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), Krebs cycle intermediates (citrate, alpha-ketoglutarate, succinate, malate), related free amino acids (glutamate, alanine), ammonia, energy store (creatine phosphate), energy mediators (ATP, ADP, AMP) and energy charge potential were evaluated. Furthermore the maximum rate (Vmax) of the following enzyme activities was evaluated in the crude extract and/or mitochondrial fraction: for the anaerobic glycolytic pathway: hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase; for the tricarboxylic acid cycle: citrate synthase, malate dehydrogenase; for the electron transfer chain: total NADH cytochrome c reductase, cytochrome oxidase. The rat gastrocnemius muscles were analysed in normoxia and after normobaric intermittent hypoxia (12 hours continuously daily; for 5 days). Cytidine and/or uridine were administered daily at the dose of 120 mg/kg, i.p., 30 min before the beginning of the experimental hypoxia. The intermittent normobaric hypoxia induced a biochemical adaptation characterized by the decrease of the muscular contents of creatine phosphate, citrate, alpha-ketoglutarate and glutamate. This adaptation occurred in the absence of significant changes in the Vmax of the tested muscle enzymes. In gastrocnemius muscle from hypoxic rats, the two biological pyrimidines tested induced various discrete, but often related, modifications of the contents of some Krebs cycle intermediates (i.e., alpha-ketoglutarate, malate) and related free amino acids (i.e., glutamate, alanine). In any case, the treatment with cytidine and/or uridine did not modify the Vmax of marker enzymes related to energy transduction.
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PMID:Modification of the skeletal muscle energy metabolism induced by intermittent normobaric hypoxia and treatment with biological pyrimidines. 402 89

In incubated colonocytes isolated from rat colons, the rates of utilization O2, glucose or glutamine were linear with respect to time for over 30 min, and the concentrations of adenine nucleotides plus the ATP/ADP or ATP/AMP concentration ratios remained approximately constant for 30 min. Glutamine, n-butyrate or ketone bodies were the only substrates that caused increases in O2 consumption by isolated incubated colonocytes. The maximum activity of hexokinase in colonic mucosa is similar to that of 6-phosphofructokinase. Starvation of the donor animal decreased the activities of hexokinase and 6-phosphofructokinase, whereas it increased those of glucose-6-phosphatase and fructose-bisphosphatase. Isolated incubated colonocytes utilized glucose at about 6.8 mumol/min per g dry wt., with lactate accounting for 83% of glucose removed. These rates were not affected by the addition of glutamine, acetoacetate or n-butyrate, and starvation of the donor animal. Isolated incubated colonocytes utilized glutamine at about 5.5 mumol/min per g dry wt., which is about 21% of the maximum activity of glutaminase. The major end-products of glutamine metabolism were glutamate, aspartate, alanine and ammonia. Starvation of the donor animal decreased the rate of glutamine utilization by colonocytes, which is accompanied by a decrease in glutamate formation and in the maximum activity of glutaminase. Isolated incubated colonocytes utilized acetoacetate at about 3.5 mumol/min per g dry wt. This rate was not markedly affected by addition of glucose or by starvation of the donor animal. When colonocytes were incubated with n-butyrate, both acetoacetate and 3-hydroxybutyrate were formed, with the latter accounting for only about 19% of total ketones produced.
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PMID:Fuel utilization in colonocytes of the rat. 407 34

1. The ability of exogenously administered cyclic AMP (adenosine 3':5'-monophosphate) to exert andromimetic action on certain carbohydrate-metabolizing enzymes was investigated in the rat prostate gland and seminal vesicles. 2. Cyclic AMP, when injected concurrently with theophylline, produced marked increases in hexokinase, phosphofructokinase, glyceraldehyde phosphate dehydrogenase, pyruvate kinase, and two hexose monophosphate-shunt enzymes, as well as alpha-glycerophosphate dehydrogenase activity in accessory sexual tissues of castrated rats. The 6-N,2'-O-dibutyryl analogue of cyclic AMP caused increases of enzyme activity that were greater than those induced by the parent compound. 3. Time-course studies demonstrated that, whereas significant increases in the activities of most enzymes occurred within 4h after the injection of cyclic AMP, maximal increases were attained at 16-24h. 4. Increase in the activity of the various prostatic and vesicular enzymes was dependent on the dose of cyclic AMP; in most instances, 2.5mg of the cyclic nucleotide/rat was sufficient to elicit a statistically significant response. 5. Administration of cyclic AMP and theophylline also produced stimulation of enzyme activities in secondary sexual tissues of immature rats. 6. Cyclic AMP and theophylline did not affect significantly any of the enzymes studied in hepatic tissue. 7. Stimulation of various carbohydrate-metabolizing enzymes in the prostate gland and seminal vesicles by cyclic AMP was independent of adrenal function. 8. Concurrent treatment with actinomycin or cycloheximide prevented the cyclic AMP- and theophylline-induced increases in enzyme activities in both castrated and adrenalectomized-castrated animals. 9. Administration of a single dose of testosterone propionate (5.0mg/100g) to castrated rats caused a significant increase in cyclic AMP concentration in both accessory sexual tissues. 10. In addition, treatment with theophylline potentiated the effects of a submaximal dose of testosterone (1.0mg/100g) on all those prostatic and seminal-vesicular enzymes that are increased by exogenous cyclic AMP. 11. The evidence indicates that cyclic AMP may be involved in triggering the known metabolic actions of androgens on secondary sexual tissues of the rat.
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PMID:Metabolic control mechanisms in mammalian systems. Involvement of adenosine 3':5'-cyclic monophosphate in androgen action. 411 Apr 60

The effects of exogenously administered 3',5'-monophosphate (cyclic AMP) on glycogen synthesis and hexose monophosphate shunt enzymes were studied in the uteri of immature and ovariectomized rats to determine whether cyclic AMP mimics the known effects of estrogenic hormones. The injection of cyclic AMP concurrently with theophylline, significantly increased the activity of uterine hexokinase, phosphofructokinase, pyruvate kinase, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and uterine glycogen content in immature rats (p less than .05). These increases were related to the dose of cyclic AMP, and as little as .2 mg was able to stimulate uterine glycogen to 169% of control values. The treatment did not significantly increase the activity of the key glycolytic or hexose monophosphate shunt enzymes in the lung and thymus, although these tissues are also not receptive to estrogen. Neither estradiol-17beta or cyclic AMP and theophylline produced any measurable effect on the uterine enzymes, isocitrate dehydrogenase, or alpha-glycerophosphate dehydrogenase. In ovariectomized and adrenalectomized-ovariectomized animals, cyclic AMP and theophylline significantly stimulated the activity of key glycolytic and hexose monophosphate shunt enzymes (p less than .05); the N6, 02-dibutyryl analog of cyclic AMP being more potent than the parent compound. Pretreatment with actinomycin or cycloheximide significantly inhibited the effects of cyclic AMP and theophylline (p less than .05), which indicates that neither cyclic AMP stimulation or the inhibition of the effects of cyclic AMP were dependent on adrenal function. The results support the possiblity that cyclic AMP may be involved in mediating the metabolic effects of estrogen on the uterus.
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PMID:Metabolic control mechanisms in mammalian systems. XV. Studies on the role of adenosine 3' ,5'-monophosphate in estrogen action on the uterus. 411 Aug 9

1. The activities of some key enzymes of glycolysis and gluconeogenesis were measured in embryonic chick, sheep and rat livers. 2. In chicken the activities of hexokinase, phosphofructokinase and pyruvate kinase are low, but those of glucose 6-phosphatase and fructose diphosphatase are very high; the converse situation exists in the rat (Burch et al. 1963), but in sheep the activities of both phosphofructokinase and fructose diphosphatase are high, and the activities of hexokinase and glucose 6-phosphatase are low. These findings are discussed in relation to carbohydrate metabolism in these embryonic livers. 3. The regulatory properties of fructose diphosphatase from the embryonic livers of these three species were compared with the properties of the enzymes from adult animals. The inhibitions by AMP and fructose diphosphate and the effects of Mg(2+) and pH on the activities of adult and foetal fructose diphosphatase are almost identical. 4. It is concluded that regulatory properties are characteristic of fructose diphosphatase from embryonic and adult tissue, and the importance of this in relation to enzyme development is discussed.
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PMID:A comparison of the properties of fructose 1,6-diphosphatase, and the activities of other key enzymes of carbohydrate metabolism, in the livers of embryonic and adult rat, sheep and domestic fowl. 429 74


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