Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose-6-phosphate dehydrogenase (EC 1.1.1.49) prepared from baker's yeast binds to immobilized Cibacron Blue F3G-A and Procion Red HE-3B. In this paper the two dyes are compared with respect to their use in the purification of this enzyme. Cibacron Blue chromatography was found useful at an early stage of purification for the removal of contaminating hexokinase, phosphoglucose isomerase and phosphoglucomutase. With Procion Red HE-3B Sepharose the NADP dependent enzymes phosphogluconate dehydrogenase and glutathione reductase are separable from glucose-6-phosphate dehydrogenase. Unlike Cibacron Blue gel chromatography, the enzyme can be specifically eluted from Procion Red HE-3B Sepharose by a NADP gradient. Other monochlorotriazine dyes like Xirone Brillant Red BHD, 4BHD, 6BHD and GHD and the dichlorotriazine dye Procion Brown MX-5BR immobilized to Sepharose have only little binding affinity to glucose-6-phosphate dehydrogenase. The binding behaviour of different immobilized triazine dyes for pre-purified and purified glucose-6-phosphate dehydrogenase is compared. In addition, the influence of the free dyes on the activity of glucose-6-phosphate dehydrogenase is studied. It is demonstrated that the results of kinetic and binding studies with the purified enzyme are not uncritically applicable for the selection of a dye as ligand for affinity chromatography during enzyme preparation.
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PMID:Interactions of immobilized and free triazine dyes with glucose-6-phosphate dehydrogenase from yeast. 351 9

Growth hormone (GH) deficiency in adults is characterized by central obesity, dyslipidemia, coagulopathy and glucose intolerance, all features of the "metabolic syndrome", explaining the increased cardiovascular morbidity and mortality associated with GH deficiency in adults. Employing the 2-step euglycemic-hyperinsulinemic clamp, we have demonstrated severe insulin resistance in GH-deficient adults, with a reduction in insulin-mediated glucose utilization of -50%. Basal glucose turnover and partitioning of whole body glucose utilization into glycolytic flux (GF) and glycogen synthesis/glucose storage (GS) pathways are normal, but insulin activation of these 2 pathways is reduced, predominantly in the GS pathway. Activation of muscle glycogen synthase by insulin is markedly decreased, as is glycogen content of muscle. Insulin-induced muscle hexokinase activity appears also to be attenuated in GH-deficient adults with raised intramuscular cellular glucose and normal-reduced concentrations of glucose-6-phosphate. Beta-cell function is not excessive in GH-deficient adults and is inappropriately low for the insulin resistance. Following treatment of GH-deficient adults with recombinant GH (rhGH), the insulin resistance is either unchanged or more pronounced by 3, 6 or 24 months of treatment, despite the significant reduction in general and central obesity. The GF and GS pathways and muscle glycogen synthase and hexokinase activities remain severely impaired. Abnormalities in free fatty acid (FFA) metabolism are present in rhGH-treated GH-deficient adults and correlate significantly with the degree of insulin resistance as do the concentrations of rhGH-induced insulin-like growth factor (IGF)-I, the post-basal insulinemia and the duration of the GHD, but is independent of obesity. In conclusion, long-term rhGH treatment in GH-deficient adults results in persistent insulin resistance and abnormalities in the GF and GS pathways due to reduced glycogen synthase and hexokinase activities, in the presence of an ongoing reduction of central obesity. We postulate that the insulin resistance is due to chronic rhGH-induced alterations in FFA metabolism, non-physiological levels of IGF-I and chronic basal hyperinsulinemia.
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PMID:Insulin sensitivity in growth hormone (GH)-deficient adults and effect of GH replacement therapy. 1044 67