Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We investigated whether the shift of cardiac myosin heavy chain (MHC) isoform observed during exposure to hypoxia is secondary to hypertrophy, or whether it is directly related to the hypoxic stress. Twelve male Wistar-Kyoto rats, 14 weeks old, were randomly assigned to two groups: sea-level control group (CO) and hypoxia group (HX). The CO group was housed 4 weeks at 1,011 hPa, and the HX group was housed for 4 weeks at 701 hPa. The expression of MHC-beta was significantly increased (600%) in the HX group as compared to the CO group in the right ventricle (p < 0.01). An increased ventricular mass induced by hypoxic exposure was associated with an increased expression of MHC-beta in the right ventricle (p < 0.05). In the left ventricle, the MHC-b expression was significantly increased (295%) in the HX group as compared to the CO group without ventricular hypertrophy (p < 0.01). No differences were observed in the adenylyl cyclase activity or in the phosphodiesterase activities in both ventricles between the CO and HX groups (p > 0.05). Oxidative enzymatic activities (citrate synthase and three-hydroxyacyl-CoA dehydrogenase) were unchanged in both ventricles following 4 weeks of hypoxia (p > 0.05). These findings suggest that, besides cardiac hypertrophy, the hypoxia-induced adaptational change to the MHC-b isoform may be mediated through a specific mechanism related to the stress of hypoxia.
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PMID:Hypoxia-induced adaptational shift in MHC-beta isoform expression in rat ventricles. 1586 34