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)

1. The preparation of rat heart mitochondria with Potter-Elvehjem homogenizer results in mitochondria showing stimualtion of respiration induced by Mg2+. This stimualtion is neither caused by adherent hexokinase nor by energy-dependent magnesium accumulation (Mg2+ content in the presence of 10 mM glutamate: 22 nmoles/mg protein; in the presence of glutamate plus antimycin A 21 nmoles/mg protein). 2. The effect of added magnesium is excluded by addition of carboxyatractyloside. This demonstrates the activity of an ATPase outside of the mitochondrial inner membrane. 3. A simple and rapid method for the preparation of Mg2+-insensitive rat heart mitochondria is presented. The minced heart is pressed through a normal syringe and then treated with trypsin. 4. A comparison of mitochondria of both preparations shows that there is no difference in magnesium content and no energy-dependent magnesium influx.
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PMID:Influence of Mg2+-ions on the properties of rat heart mitochondria in dependence on the preparation. 70 27

The kinetic properties of hexokinase of L1210 ascites tumor cells propagated in DBA/2HaD mice are altered by treatment of the mice with the modified nucleoside N6-(delta2-isopentenyl)-adensone (IPA). Relative to animals not treated with IPA, ascites cell hexokinase showed an increased affinity for ATP and a decreased affinity for glucose as a result of IPA treatment. The heat stability of the enzyme was different in treated and untreated mice. It was concluded that IPA treatment may either produce changes in enzyme conformation which resulted in a change in control mechanisms or may induce the formation of a hexokinase isoenzyme.
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PMID:Effect of N6-(delta2-isopentenyl)adenosine treatment in vivo on hexokinase activity of mouse L 1210 cells. 105 42

The effects of insulin on carbohydrate metabolism in atrophied rat soleus muscle are increased after unweighting by tail-cast suspension. This work has been extended by testing the effect of unweighting on the response of carbohydrate metabolism to isoproterenol, a beta-adrenergic agonist. Isoproterenol promoted glycogen degradation more in the unweighted than in the weight-bearing soleus but showed no differences in the extensor digitorum longus, which is unresponsive to hindlimb unweighting. In soleus muscles depleted of glycogen, to avoid varied inhibitory effects of glycogen on glycogen synthesis, isoproterenol inhibited this process more in the unweighted muscle. Isoproterenol did not have a greater inhibitory effect on net uptake of 2-deoxy-D[1,2-3H]glucose by the unweighted muscle. Measurements of intracellular 2-deoxy-[3H]glucose 6-phosphate and 3-O-methyl-D-[1-3H]glucose, which cannot be phosphorylated, showed that isoproterenol inhibited glucose phosphorylation but not transport. This effect could be explained by an increase of glucose 6-phosphate, an inhibitor of hexokinase. At 100 microU insulin/ml but not at a lower amount (10 microU/ml), isoproterenol inhibited hexose phosphorylation more in the control than in the unweighted muscle. This result may be explained by greater insulin antagonism in the unweighted muscle owing to increased insulin sensitivity. However, insulin antagonism of isoproterenol stimulation of glycogenolysis or inhibition of glycogenesis was not altered by unweighting. Therefore, for some aspects of carbohydrate metabolism, the unweighted muscle has an increased response to beta-adrenergic activation, just as this muscle shows increased responses to insulin.
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PMID:Beta-adrenergic effects on carbohydrate metabolism in the unweighted rat soleus muscle. 207 8

Pathological conditions or nutrient deprivation in the heart cause an imbalance between rates of protein synthesis and degradation, often resulting in a severe depletion of cardiac protein. We used cultured neonatal rat heart cells, a model system exhibiting positive nitrogen balance, to examine the effects of 10 h of starvation on myocardial glucose and protein metabolism. Cellular capacity for glucose utilization was depressed after starvation, as evidenced by lower hexokinase and other glycolytic enzyme activities and a 21% decrease in glucose usage. A 21.0% decrease in protein synthetic rate and an increase in protein degradation rate combined to yield a 29.5% decrease in total cellular protein during starvation. Degradation rates increased 29.0, 46.7, and 59.6% in 2-, 24-, and 96-h prelabeled cells, respectively, indicating that lability increased with half-life of proteins. During refeeding of starved, cultured cells, at least three proteins were synthesized at a lower rate. At the same time, proteins with approximate molecular masses of 45, 84, 92, and 174 kDa exhibited increased synthesis.
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PMID:Protein metabolism during nutrient deprivation and refeeding of neonatal heart cells. 259 85

The hexokinases, by converting glucose to glucose-6-phosphate, help maintain the downhill gradient that results in movement of glucose into cells through the facilitative glucose transporters. GLUT4 and hexokinase (HK) II are the major transporter and hexokinase isoforms in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. To understand whether hormones influence the contribution of phosphorylation to cellular glucose utilization, we investigated the effects that catecholamines, cyclic AMP (cAMP), and insulin have on HKII gene expression in cells representative of muscle (L6 cells) and brown (BFC-1B cells) and white (3T3-F442A cells) adipose tissues. Isoproterenol or the cAMP analog 8-chlorophenylthio-cAMP selectively increase HKII gene transcription in L6 cells, as does insulin (Printz RL, Koch S, Potter LP, O'Doherty RM, Tiesinga JJ, Moritz S, Granner DK: Hexokinase II mRNA and gene structure, regulation by insulin, and evolution. J Biol Chem 268:5209-5219, 1993), and cause a concentration- and time-dependent increase of HKII mRNA in both muscle and fat cell lines without changing HKI mRNA. Isoproterenol and insulin also increase the rate of synthesis of HKII protein and increase glucose phosphorylation and glucose utilization in L6 cells.
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PMID:Regulation of hexokinase II gene transcription and glucose phosphorylation by catecholamines, cyclic AMP, and insulin. 758 50

Hexokinases catalyze the phosphorylation of glucose and initiate cellular glucose metabolism. Hexokinase II (HKII) is the principal hexokinase isoform in skeletal muscle, heart, and adipose tissue. Isoproterenol and exogenous cyclic AMP (cAMP) increase HKII gene transcription in L6 myotubes. Various segments of the HKII promoter that direct the expression of the chloramphenicol acetyltransferase reporter gene were transfected into L6 myotubes to identify basal and cAMP response elements. The 5'-flanking region that extends 90 base pairs upstream of the transcription start site includes a CCAAT box and a cAMP response element (CRE); both contribute to basal promoter activity and each provides an independent, maximal response to cAMP. An inverted CCAAT motif, or Y box, located just upstream of the CCAAT box, contributes to basal promoter activity but is not involved in the cAMP response. Homo- and heterodimers composed of the CRE-binding protein and activating transcription factor-1 bind specifically to the CRE. The Y box and the CCAAT box specifically bind the factor NF-Y (also known as CBF).
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PMID:Identification and characterization of basal and cyclic AMP response elements in the promoter of the rat hexokinase II gene. 866 88

This study tested the hypothesis that alterations in the metabolic integrity of grafted muscle contribute to its diminished ability to sustain power. Compared with control muscles, muscles studied 120 days after the grafting procedure had lower specific force and sustained power. The sustained power protocol resulted in a depletion of muscle glycogen in control (83%) and grafted (85%) animals. Grafts had lower pre- and poststimulation glycogen, diminished citrate synthase activity, and greater hexokinase activity. No differences were observed in phosphofructokinase activity, glucose transporter GLUT-4 content, fiber type, beta-adrenergic-receptor (beta-AR) density, or binding affinity. Isoproterenol-stimulated adenylyl cyclase activity was lower in grafted vs. control muscle, suggesting an uncoupling of the beta-AR-effector complex. Thus the diminished ability of the grafted muscle to sustain power may be explained, in part, by a decrease in energy available from glycogen stores and/or a decrease in oxidative capacity.
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PMID:Functional deficits in medial gastrocnemius grafts in rats: relation to muscle metabolism and beta-AR regulation. 921 46