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 purification of an enzyme is described, a protease, from human erythrocytes which degrades insulin with a high specificity at physiological hormone concentrations. Since the enzyme contains free sulfhydryl groups, affinity chromatography on organomercuri-Sepharose proved to be applicable as a valuable step in the isolation procedure. The purification factor amounted to approx. 6000, the yield to 8%. 1mg of purified enzyme was capable of degrading 50 pmol of insulin/min into trichloroacetic acid-soluble split products. The purified insulin-degrading enzyme was shown to be homogeneous, as demonstrated by gel chromatography, gel electrophoresis and isoelectric focusing. The isoelectric points was at pH 5.8. The molecular weight of nativ enzyme was estimated by gel chromatography and gel electrophoresis and found to be about 150 000-160 000, consisting of 4 subunits. Degradation products of insulin eluted from a Biogel P 30 column are smaller than the A-chain of the hormone, suggesting the activity of a protease. The enzyme appears to be specific for insulin in that it does not degrade other peptide hormones such as growth hormone, prolactin, or thyroid-stimulating hormone. Furthermore, the enzyme does not inactivate enzymes such as lactate dehydrogenase, aldolase, fructose 1,6-bisphosphatase, hexosephosphate isomerase or hexokinase.
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PMID:Purification to homogeneity of an insulin-degrading enzyme from human erythrocytes. 699 71

1. Addition of glucose induced an inactivation of mitochondrial enzymes in the yeast Saccharomyces cerevisiae containing normal mitochondrial particles. 2. The glucose-induced inactivation of mitochondrial enzymes was inhibited by the presence of cycloheximide. 3. Pepstatin also inhibited the inactivation, but phenylmethanesulphonyl fluoride accelerated the inactivation. 4. The specific activities of fructose 1,6-bisphosphatase and cytoplasmic malate dehydrogenase were decreased on the exposure to glucose, as well as those of the mitochondrial enzymes. However, the glucose-induced inactivation of cytoplasmic enzymes was not inhibited by the presence of pepstatin. 5. The specific activities of hexokinase and phosphofructokinase, which are cytoplasmic enzymes were increased by the addition of glucose, and this effect was not affected by pepstatin. 6. Addition of glucose resulted in an increase in the synthesis of proteins of the mitochondria and the cytosol, and simultaneously in degradation of these mitochondrial and cytoplasmic proteins.
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PMID:Glucose-induced inactivation of mitochondrial enzymes in the yeast Saccharomyces cerevisiae. 703 27

Galactosamine-induced hepatitis caused a marked increase in plasma lactate and pyruvate, but completely abolished the increase in ketone bodies in the rat exposed to an 8000 m simulated altitude. Plasma free fatty acid as the precursor of ketone bodies was higher in the galactosamine-treated rats during and after an exposure to 8000 m altitude. Treatment of the rat with galactosamine markedly reduced activities of citrate synthase, fumarase, glutamate dehydrogenase and fructose 1,6-bisphosphatase, but increased hexokinase and glucose 6-phosphate dehydrogenase in the liver. The effect of galactosamine-induced hepatitis on the energy metabolism can be explained by a reduction of mitochondrial oxidative enzymes and gluconeogenesis, and involves a shift of the aerobic metabolism to anaerobic glycolysis at high altitude.
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PMID:Effect of galactosamine-induced hepatitis on the aerobic and anaerobic metabolism of the rat exposed to high-altitude hypoxia. 774 7

The observation that the level of S-thiolated proteins (protein-thiol mixed disulfides) was transiently increased in the lens epithelial cells correlation with the transient inactivation of glyceraldehyde-3-phosphate dehydrogenase (G-3PD), a key glycolytic enzyme, when the cells were treated with a bolus of hydrogen peroxide, prompted our speculation that G-3PD may have been transiently thiolated at the SH sensitive active center. In the meantime, thioltransferase (TTase), a thiol regulating enzyme, whose activity remained constant under the same condition, may be regulating G-3PD and other sulfhydryl-sensitive glycolytic enzymes through thiol-disulfide exchange reactions ( Lou et al., 1998 ). To prove this hypothesis, several purified glycolytic enzymes from a commercial source, including hexokinase (HK), G-3PD, pyruvate kinase (PK) and fructose 1,6-bisphosphatase (FBPase), an enzyme in gluconeogenesis, were made into protein-thiol mixed disulfide and used for this study. Glycolytic enzymes in cultured rabbit lens epithelial cells pre-exposed to H(2)O(2)(0.5 m M for 15 min) were also studied for this purpose. Recombinant human lens thioltransferase (RHLT), which was isolated and purified previously in this laboratory, reactivated these pure glycolytic enzymes inactivated by forming protein-S-S-gluthathione (PSSG), protein-S-S-cysteine (PSSC) or, protein-S-S-cysteamine after thiolating with oxidized glutathione, cystine or cystamine respectively. RHLT also reactivated these enzymes in the cell extract of cultured rabbit lens epithelial cells after being briefly exposed to 0.5 m M H(2)O(2). The S-thiolation and dethiolation of FBPase however, showed an opposite effect to that of glycolytic enzymes. These results suggest that TTase may participate in the repair process of glycolytic enzymes during oxidative stress and restore their activities in situ.
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PMID:Modulation of lens glycolytic pathway by thioltransferase. 1084 79

The dauer larva, a non-feeding and developmentally arrested stage of the free-living nematode Caenorhabditis elegans, is morphologically and physiologically specialized for survival and dispersal during adverse growth conditions. The ability of dauer larvae to live several times longer than the continuous developmental life span has been attributed in part to a repressed metabolism. We used serial analysis of gene expression (SAGE) profiles from dauer larvae and mixed growing stages to compare expression patterns for genes with known or predicted roles in glycolysis, gluconeogenesis, glycogen metabolism, the Krebs and glyoxylate cycles, and selected fermentation pathways. Ratios of mixed:dauer transcripts indicated non-dauer enrichment that was consistent with previously determined adult:dauer enzyme activity ratios for hexokinase (glycolysis), phosphoenolpyruvate carboxykinase and fructose 1,6-bisphosphatase (gluconeogenesis), isocitrate dehydrogenase (NADP-dependent), and isocitrate lyase-malate synthase (glyoxylate cycle). Transcripts for the majority of Krebs cycle components were not differentially represented in the two profiles. Transcript abundance for pyruvate kinase, alcohol dehydrogenase, a putative cytosolic fumarate reductase, two pyruvate dehydrogenase components, and a succinyl CoA synthetase alpha subunit implied that anaerobic pathways were upregulated in dauer larvae. Generation of nutritive fermentation byproducts and the moderation of oxidative damage are potential benefits of a hypoxic dauer interior.
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PMID:SAGE surveys C. elegans carbohydrate metabolism: evidence for an anaerobic shift in the long-lived dauer larva. 1287 42

Eclipta alba, an indigenous medicinal plant, has a folk (Siddha and Ayurvedha) reputation in rural southern India as a hypoglycemic agent. In order to confirm this claim, the present study was carried out to evaluate the antihyperglycemic effect of E. alba and to study the activities of liver hexokinase and gluconeogenic enzymes such as glucose-6-phosphatase and fructose 1,6-bisphosphatase in the liver of control and alloxan-diabetic rats. Oral administration of leaf suspension of E. alba (2 and 4 g/kg body weight) for 60 days resulted in significant reduction in blood glucose (from 372.0 +/- 33.2 to 117.0 +/- 22.8), glycosylated hemoglobin HbA(1)c, a decrease in the activities of glucose-6 phosphatase and fructose 1,6-bisphosphatase, and an increase in the activity of liver hexokinase. E. alba at dose of 2 g/kg body weight exhibited better sugar reduction than 4 g/kg body weight. Thus, the present study clearly shows that the oral administration of E. alba possess potent antihyperglycemic activity.
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PMID:Antihyperglycemic activity of Eclipta alba leaf on alloxan-induced diabetic rats. 1536 23

The present study investigates the effect of oral administration of an aqueous Enicostemma littorale whole plant extract on some key carbohydrate metabolic enzymes and antioxidant defence in alloxan-induced diabetes in rats. Rats were rendered diabetic by alloxan (150 mgkg(-1) body weight) administration. Oral administration of E. littorale extract for 45 days increased the activity of hexokinase and decreased the activities of glucose 6-phosphatase and fructose 1,6-bisphosphatase significantly in the serum, liver and kidney of diabetic rats. The extract lowered the concentration of thiobarbituric acid reactive substances and lipid hydroperoxides significantly in brain and increased it significantly in heart in diabetic rats. E. littorale administration increased the concentration of reduced glutathione and the activity of glutathione peroxidase in diabetic rats. The activities of superoxide dismutase and catalase were increased significantly by E. littorale treatment in diabetic rats. The effect of a 2 g kg(-1) dose was greater than that of a 1 gkg(-1) dose. Insulin (6 units kg(-1)) normalized all the parameters in diabetic rats. Our study has provided evidence for the antidiabetic activity of E. littorale aqueous extract. This study can also be extrapolated to clinical studies in future.
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PMID:Effect of aqueous Enicostemma littorale Blume extract on key carbohydrate metabolic enzymes, lipid peroxides and antioxidants in alloxan-induced diabetic rats. 1583 Dec 11

The purpose of the study was to assess in female fish the possible interaction between treatment with a polycyclic aromatic hydrocarbon (PAH) like naphthalene and the onset of vitellogenesis. In a first experiment, female rainbow trout (Oncorhynchus mykiss) at stages 2-3 (previtellogenesis) or 4 (early vitellogenesis) were intraperitoneally injected (2 microl g(-1)) with vegetable oil alone (control) or containing naphthalene (50 mg kg(-1)) to be sampled 3 h later. A second experiment was similarly designed but using fish intraperitoneally implanted (10 microl g(-1)) with slow-release coconut oil implants alone (control) or containing 50 mg naphthalene kg(-1) body mass that were sampled 3 days after injection. On each sampling time, plasma levels of cortisol and 17beta-estradiol, and several metabolic parameters in plasma, liver and gonad were assessed. In controls, early vitellogenic fish compared with previtellogenic fish displayed changes that in some cases are confirmatory of previous studies whereas in other cases provide new information in plasma (increased amino acid levels), liver (decreased capacity for exporting glucose and reduced amino acid levels) and gonad (decreased amino acid levels). Naphthalene treatment produced in previtellogenic fish decreased 17beta-estradiol levels in plasma, increased plasma glucose or decreased liver gluconeogenic capacity whereas no major effects were noticed on parameters involved in lipid, amino acid and lactate metabolism. Differential effects of naphthalene treatment were noticed in early vitellogenic fish such as decreased 17beta-estradiol and glucose levels in plasma, increased hexokinase and glucokinase and lack of changes in fructose 1,6-bisphosphatase activities in liver, and a lower decrease of amino acid levels in gonad. Those alterations produced by naphthalene treatment resulted in a decreased capacity for covering the energy demand of vitellogenesis in liver and gonad that could contribute to a delay and/or impairment of the onset of maturation.
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PMID:Interactive effects of naphthalene treatment and the onset of vitellogenesis on energy metabolism in liver and gonad, and plasma steroid hormones of rainbow trout Oncorhynchus mykiss. 1695 43

We assessed the daily patterns of parameters involved in energy metabolism in liver, white muscle, and gills of rainbow trout. Where daily rhythms were found, we analyzed the potential influence of feeding. Immature rainbow trout were randomly distributed in 3 groups: fish fed for 7 days, fish fasted for 7 days, and fish fasted for 7 days and refed for 4 days. On sampling day, fish of fed and refed groups were fed at 11.00 h, and all fish were sampled from each treatment group using the following time schedule: 14.00, 18.00, 21.00, 00.00, 04.00, 07.00, 10.00 and 14.00 h. The results obtained from metabolic parameters can be grouped into four different categories, such as i) those displaying no daily changes in any group assessed in liver (acetoacetate and lactate levels), white muscle (protein levels, and low Km (glucose) hexokinase (HK) and HK-IV activities) and gills (protein levels), ii) those displaying no 24 h changes in fed fish but in refed or fasted fish in liver (glucose, glycogen, amino acid and protein levels, and HK-IV activity), white muscle (glycogen and amino acid levels) and gills (glucose levels), iii) those displaying 24 h changes that were apparently dependent on feeding since they disappear in fasted fish in liver (Low Km (glucose) HK, lactate dehydrogenase (LDH-O), glucose 6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FBPase) , alpha-glycerophosphate dehydrogenase (G3PDH), glutamate dehydrogenase (GDH) and aspartate aminotransferase (Asp-AT) activities), white muscle (glucose levels, and pyruvate kinase (PK), LDH-O, G3PDH and Asp-AT activities) and gills (glycogen and lactate levels, and Low Km (glucose) HK, HK-IV, LDH-O and Asp-AT activities), and iv) those parameters displaying 24 h changes apparently not dependent on feeding in liver (lactate levels and PK activity) and gills (amino acid levels, and PK and GDH activities). In general, most 24 h changes observed were dependent on feeding and can be also related to daily changes in activity.
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PMID:Daily changes in parameters of energy metabolism in liver, white muscle, and gills of rainbow trout: dependence on feeding. 1731 50

The present study is an investigation into the role of quercitrin on carbohydrate metabolism in normal and streptozotocin (STZ)-induced diabetic rats. Administration of STZ leads to a significant increase (P < 0.05) in fasting plasma glucose and a decrease in insulin levels. The content of glycogen is significantly decreased (P < 0.05) in liver and muscle, but increased in the kidney. The activity of hexokinase decreased whereas the activities of glucose 6-phosphatase and fructose 1,6-bisphosphatase significantly increased (P < 0.05) in the tissues. Oral administration of quercitrin (30 mg/kg) to diabetic rats for a period of 30 days resulted in significant (P < 0.05) alterations in the parameters studied but not in normal rats. A decrease of plasma glucose and increase in insulin levels were observed along with the restoration of glycogen content and the activities of carbohydrate metabolic enzymes in quercitrin-treated diabetic rats. The histopathological study of the pancreas revealed the protective role of quercitrin. There was an expansion of the islets and decreased fatty infiltrate of the islets in quercitrin treated diabetic rats. In normal rats treated with quercitrin, we could not observe any significant change in all the parameters studied. Combined, these results show that quercitrin plays a positive role in carbohydrate metabolism and antioxidant status in diabetic rats.
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PMID:Quercitrin, a bioflavonoid improves glucose homeostasis in streptozotocin-induced diabetic tissues by altering glycolytic and gluconeogenic enzymes. 1968 49


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