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:2.3.3.1 (citrate synthase)
4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared responses of the fast extensor digitorum longus (EDL) and tibialis anterior (TA) muscles in young (15-week) and aging (101-week) male Brown Norwegian rats to 50 days of chronic low-frequency stimulation (CLFS, 10 Hz, 10 hours/day). After 50 days of CLFS, the EDL muscles of the young (22-week) and aging (108-week) rats displayed similar increases in type IIA fibers, relative concentration of myosin heavy chain MHCIIa, elevations in mitochondrial citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities, and similar decreases in glycolytic enzyme activities (glyceraldehydephosphate dehydrogenase, lactate dehydrogenase). TA muscle in young rats contained a few cytochrome c oxidase negative (COX-) type I fibers. Their number was approximately 2-fold elevated by CLFS. Conversely, aging muscle, which contained a slightly higher amount of COX- fibers than young TA muscle, responded to CLFS with a significant decrease in COX- fibers. The appearance of small COX-positive type I fibers in stimulated aging muscle indicated that regenerating type I fibers "diluted" the COX-deficient fiber population.
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PMID:Adaptive potentials of skeletal muscle in young and aging rats. 1191 26

We tested the hypothesis that chronic endurance exercise is associated with the recruitment of four major upper airway muscles (genioglossus, digastric, sternohyoid, and omohyoid) and results in an increased oxidative capacity and a fast-toward-slow shift in myosin heavy chain (MHC) isoforms of these muscles. Female Sprague-Dawley rats (n = 8; 60 days old) performed treadmill exercises for 12 weeks (4 days/week; 90 minutes/day). Age-matched sedentary female rats (n = 10) served as control animals. Training was associated with an increase (p < 0.05) in the activities of both citrate synthase and superoxide dismutase in the digastric and sternohyoid muscles, as well as in the costal diaphragm. Compared with the control animals, Type I MHC content increased (p < 0.05) and Type IIb MHC content decreased (p < 0.05) in the digastric, sternohyoid, and diaphragm muscles of exercised animals. Training did not alter (p > 0.05) MHC phenotype, oxidative capacity, or antioxidant enzyme activity in the omohyoid or genioglossus muscle. These data indicate that endurance exercise training is associated with a fast-to-slow shift in MHC phenotype together with an increase in both oxidative and antioxidant capacity in selected upper airway muscles. It seems possible that this exercise-mediated adaptation is related to the recruitment of these muscles as stabilizers of the upper airway.
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PMID:Adaptation of upper airway muscles to chronic endurance exercise. 1215 59

We evaluated the effects of testosterone overload on mitochondrial superoxide dismutase (MnSOD), cytochrome oxidase (COX) and citrate synthase (CS) activities of the rat superficial gastrocnemius both in non-exercised muscle and following moderate endurance training. Basal (bLPO) and stimulated (sLPO) lipid peroxidation was measured as an index of oxidative tissue damage. Furthermore, to assess the relationship between exercise and testosterone-induced metabolic adaptations and contractile protein expression, the distribution of myosin heavy chain (MHC) isoforms was analysed by SDS-PAGE. Samples were obtained from: controls (C), rats treated with testosterone propionate (Tp) (TP, 5 mg kg(-1) i.m. 6 days/week), trained rats (E, 5 days/week) and rats trained and treated with Tp (ETP). MnSOD significantly increased in E and TP in comparison with C and ETP. Training induced a significant increase in COX activity both in E and ETP whereas a statistical reduction was observed in TP in comparison with the other groups. Moreover, testosterone administration was associated with a significant reduction in CS activity which significantly increased in ETP. A reduction in lipid peroxidation was observed in E and ETP in comparison with controls both in basal and stimulated conditions, whereas TP showed a significant increase of bLPO. In trained rats enzymatic changes were correlated with an increase in the proportion of fast oxidative MHC-2A and MHC-2X with decrease of the proportion of fast MHC-2B. In contrast, Tp treatment induced an increase in the proportion of MHC-2B whereas MHC-2A and MHC-2X disappeared. Finally, ETP showed a reduction in MHC-2B and an increase in MHC-1 and MHC-2X. These data suggest that testosterone supplementation seems not to significantly modify the metabolic adaptation induced by exercise in gastrocnemius muscle. Furthermore, testosterone overload to non-exercised rats seems to reduce the mitochondrial function and increase the lipid peroxidation of the muscle.
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PMID:"Oxidative stress": effects of mild endurance training and testosterone treatment on rat gastrocnemius muscle. 1235 95

Neuromuscular electrical stimulation has grown in popularity as a therapeutic device for training and an ambulation aid to human paralyzed muscle. Despite its current clinical use, few studies have attempted to concurrently investigate the functional and intramuscular adaptations which occur after electrical stimulation training. Six individuals with a spinal cord injury performed 10 weeks of electrical stimulation leg cycle training (30 min d(-1), 3 d week(-1)). The paralyzed vastus lateralis muscle showed significant alterations in skeletal muscle characteristics after the training, indicated by an improvement in total work output (52-112 kJ; P < 0.05), an increase in fiber cross-sectional area (18 to 41 x 10(2) microm(2); P < 0.05), a reduction in the percentage of type IIX fibers (75% to 12%; P < 0.05), a decrease in myosin heavy chain IIx (68% to 44%; P < 0.05), an increase in capillary density (2-3.5 capillaries around fiber; P < 0.05) and increases in activity levels of citrate synthase (7-16 mU mg(-1) protein) and hexokinase (1.2-2.4 mU mg(-1) protein). This study showed that 10 weeks of electrical stimulation training of human paralyzed muscle induces concurrent improvements in functional capacity and oxidative metabolism.
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PMID:Effects of electrical stimulation-induced leg training on skeletal muscle adaptability in spinal cord injury. 1238 78

We examined the effects of undernutrition on muscle development during the first postnatal week in pigs. Eighteen piglets were subjected to three nutritional levels (300, 200 or 100 g/(kg body. d) of colostrum then milk) between birth and slaughter at 7 d of age. Longissimus lumborum (LL), a fast-twitch glycolytic muscle, and rhomboideus (RH), a mixed slow- and fast-twitch oxido-glycolytic muscle, were taken for myofiber typing and biochemical analyses. Enzyme activities of lactate dehydrogenase (LDH), citrate synthase (CS) and beta-hydroxy-acyl-CoA-dehydrogenase (HAD) were used as markers of glycolytic, oxidative and lipid beta-oxidation capacities, respectively. Undernutrition selectively decreased (P < 0.001) hypertrophy of the future fast-twitch glycolytic fibers in LL. Contractile and metabolic maturation was delayed in the later maturing LL, as reflected by a decrease in muscle protein concentration (P < 0.01), an increase (P < 0.05) in the percentage of myofibers still expressing the fetal myosin heavy chain (MyHC), a lower postnatal increase in LDH activity (P < 0.001) and a delayed decrease in the percentage of IIa MyHC positive fibers (P < 0.001). Otherwise, restriction tended (P < 0.10) to increase the percentage of slow type I MyHC containing fibers in both muscles and of alpha-cardiac MyHC positive fibers in RH (P < 0.05). The LDH/CS ratio decreased dramatically (P < 0.001) after restriction, to a greater extent in LL than in RH. These changes denoted a more oxidative metabolism using fewer carbohydrates and more lipids in restricted pigs, as suggested by the increased activity of HAD (P < 0.001) and decreased respiratory quotient (P < 0.001).
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PMID:Early postnatal food intake alters myofiber maturation in pig skeletal muscle. 1251 81

The present study was undertaken to investigate in a randomized controlled trial the effects of chronic (10 weeks, 4 h per day, 7 days per week) low-frequency (15 Hz) stimulation (CLFS) of the knee extensor and hamstring muscles of both legs in healthy volunteers via surface electrodes. A control group (n=10) underwent the same treatment (sham stimulation) as the CLFS-treated group (n=10), except that stimulation intensity was kept at a level which did not evoke contractions. Biopsy samples were taken before the onset and after cessation of stimulation from the right vastus lateralis muscle of all subjects. The biopsy samples were analyzed for changes in myosin heavy chain (MHC) isoforms and activities of citrate synthase (CS) and glyceraldehyde phosphate dehydrogenase (GAPDH) as markers of aerobic-oxidative and anaerobic pathways of energy metabolism, respectively. In addition, functional properties, i.e., oxygen consumption (VO(2)) and work capacity, were assessed. Sham stimulation did not affect the functional properties and had no detectable effect on MHC isoform and enzyme activity patterns. Conversely, CLFS induced changes in the MHC isoform pattern in the fast-to-slow direction with an approximately 20% decrease in the relative concentration of MHCIId/x (from 28% to 22%) and an approximately 10% increase in the relative concentration of MHCI (from 30% to 34%). In addition, CLFS led to a approximately 9% increase in the activity of CS concomitant with an approximatley 7% decrease in the activity of GAPDH. This increase in aerobic-oxidative capacity was accompanied by improved work capacity and VO(2) at the anaerobic threshold by 26% and 20%, respectively.
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PMID:Functional and biochemical properties of chronically stimulated human skeletal muscle. 1266 86

The present study examined the effect of chronic activation of 5'-AMP-activated protein kinase (AMPK) on the metabolic profile, including uncoupling protein-3 (UCP-3) and myosin heavy chain (MHC)-based fibre phenotype of rodent fast-twitch tibialis anterior muscle. Sprague-Dawley rats were given daily injections of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), a known activator of AMPK, or vehicle (control) for 28 days. After AICAR treatment, UCP-3 expression at the mRNA level was elevated 1.6 +/- 0.1-fold (P < 0.006) and corresponded to a 3.3 +/- 0.2-fold increase in UCP-3 protein content (P < 0.0001). In addition, the activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial volume density, were elevated 1.6-fold (P < 0.006), while the activity of lactate dehydrogenase (EC 1.1.1.27) was reduced to 80 % of control (P < 0.02). No differences were detected after AICAR treatment in the activities of the glycolytic reference enzymes glyceraldehydephosphate dehydrogenase (EC 1.2.1.12) or phosphofructokinase (EC 2.7.1.11), nor were MHC-based fibre-type transitions observed, using immunohistochemical or electrophoretic analytical methods. These changes could not be attributed to variations in inter-organ signalling by metabolic substrates or insulin. We conclude that an AMPK-dependent pathway of signal transduction does mimic some of the metabolic changes associated with chronic exercise training, but does not affect expression of the MHC-based structural phenotype. Thus, the metabolic and MHC-based fibre types do not appear to be regulated in a co-ordinated way, but may be independently modified by different signalling pathways.
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PMID:AMPK activation increases uncoupling protein-3 expression and mitochondrial enzyme activities in rat muscle without fibre type transitions. 1281 56

To investigate the effects of microgravity on murine skeletal muscle fiber size, muscle contractile protein, and enzymatic activity, female C57BL/6J mice, aged 64 days, were divided into animal enclosure module (AEM) ground control and spaceflight (SF) treatment groups. SF animals were flown on the space shuttle Endeavour (STS-108/UF-1) and subjected to approximately 11 days and 19 h of microgravity. Immunohistochemical analysis of muscle fiber cross-sectional area revealed that, in each of the muscles analyzed, mean muscle fiber cross-sectional area was significantly reduced (P < 0.0001) for all fiber types for SF vs. AEM control. In the soleus, immunohistochemical analysis of myosin heavy chain (MHC) isoform expression revealed a significant increase in the percentage of muscle fibers expressing MHC IIx and MHC IIb (P < 0.05). For the gastrocnemius and plantaris, no significant changes in MHC isoform expression were observed. For the muscles analyzed, no alterations in MHC I or MHC IIa protein expression were observed. Enzymatic analysis of the gastrocnemius revealed a significant decrease in citrate synthase activity in SF vs. AEM control.
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PMID:Skeletal muscle adaptations to microgravity exposure in the mouse. 1288 90

Previous studies suggested that administration of cyclosporin A (CsA), an immunosuppressive agent, contributes to the increased fatigability of heart transplant recipients. The aim of this study was to investigate whether CsA itself, without vehicle, affects the function of mitochondria maintained in situ, in rats treated with CsA (25mg/kg/day) dissolved in ethanol and olive oil. Treatment with CsA induced a 16% decrease in slow myosin heavy chain (MHC) associated with a 225% increase in fast MHCIIa. The proportion of fibers expressing type IIa MHC increased as a result of CsA treatment. Soleus from the CsA-treated animals showed an increase in both basal (+85%) and maximal (+37%) mitochondrial respiration (P < 0.001), consistent with a 24% increase in citrate synthase activity, whereas the apparent Km for adenosine diphosphate was unchanged. By itself, CsA has no deleterious effects on muscle oxidative capacity but induces alterations in energy metabolism in accordance with the increased proportion of fast-twitch oxidative fibers.
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PMID:Cyclosporin A treatment increases rat soleus muscle oxidative capacities. 1292 92

This study was designed to characterize cardiac changes in myosin heavy chain (MHC)-beta, capacity for oxidative metabolism and muscle mass in hearts of rats born and raised at simulated altitudes (2200 m or 4000 m) compared to age-matched sea level controls. On the basis of electrophoretic analyses, we found that the hypoxia-induced ventricular hypertrophy produces a significant increase in MHC-beta in both ventricles. Furthermore, we observed an exponential relationship between the mass of right ventricular muscle and percentages in the expression of MHC-beta (r=0.928, P<0.001). We also observed the reduction in the citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD) activities in both hypertrophied ventricles (P<0.001). As a consequence, there were negative correlations between the percentage expression of MHC-beta and the CS or HAD activities (P<0.001). In contrast, there were no significant correlations between the relative expressions of MHC-beta and either CS or HAD enzymatic activities in both ventricles after adjusting for the relative wet mass. In conclusion, the observed increases in MHC-beta may be a compensation to augment efficiency if muscles contract in hypertrophied hearts where mitochondria fail to respond to increases in tissue mass. These findings suggest that the increased relative expression of MHC-beta is a compensation to sustain cardiac contractile efficiency in response to impaired oxidative metabolism in the hypoxia-induced hypertrophied ventricles of rats.
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PMID:Alterations in the expression of myosin heavy chain isoforms in hypoxia-induced hypertrophied ventricles in rats. 1294 47


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