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)

The present study compares the time courses of the early changes in parvalbumin content, in the properties of the sarcoplasmic reticulum (SR) and in activity and isozyme patterns of metabolic enzymes in chronically (12 h/day) stimulated fast twitch tibialis anterior (TA) muscle of the rabbit. Under the chosen conditions of stimulation, the first significant changes appeared after 6 days. Except for the delayed reduction in pyruvate kinase, the time course of the changes were the same. After 14 days of stimulation, parvalbumin decreased to 37% and Ca2+-ATPase activity of the SR to 29% of normal values. The transformation of the SR was also reflected by a 64% decrease of the 115000-Mr Ca2+-pumping peptide and a 5-fold increase in a 30000-Mr peptide. Following an identical time course, the mitochondrial activities of citrate synthase, 3-hydroxyacyl-CoA dehydrogenase and ketoacid-CoA transferase increased 2.9, 3.0 and 3.7-fold respectively. A similar time course was observed in the M to H-type transition of the lactate dehydrogenase isozymes. The cause of these changes is discussed as it relates to altered transcriptional and/or translational activities. It is suggested that an increase in free intracellular Ca2+ caused by increased contractile activity, which is then perpetuated by the decrease in Ca2+-binding and sequestering capacities, might be the signal for such altered synthetic activities.
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PMID:Relationships between early alterations in parvalbumins, sarcoplasmic reticulum and metabolic enzymes in chronically stimulated fast twitch muscle. 622 11

During seasonal acclimatization in white-footed mice (Peromyscus leucopus), there is a substantial increase in the capacity for aerobic heat production under cold stress (Mmax) in winter animals. The possibility that increases in levels of enzymes involved in aerobic heat production could be responsible for the increase in Mmax was investigated in mice captured in summer and winter. Activities of citrate synthase (CS) and beta-hydroxyacyl-CoA dehydrogenase (HOAD) and concentrations of cytochrome c (cyt c) were measured in the two primary thermogenic tissues of small mammals, skeletal muscle and brown adipose tissue (BAT). Additionally, cyt c was measured in heart, liver, and whole-body samples. CS and cyt c were used as indicators of aerobic capacity, and HOAD was used to indicate the capacity for beta-oxidation. In winter CS, cyt c, and HOAD increased (expressed per g wet mass) in skeletal muscle and BAT. There was an increase in cyt c of whole-body samples, liver, and skeletal muscle of between 55 and 78%, but no change was observed in cardiac tissue. There was an approximately 80% increase in CS and HOAD in skeletal muscle. The highly aerobic nature of BAT and its primary role in heat production are supported by the high activities in summer animals and the increase observed in winter (200, 1,570, and 220% increase in CS, HOAD, and cyt c, respectively).
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PMID:Seasonal changes in enzymes of aerobic heat production in the white-footed mouse. 626 12

NADH:ubiquinone reductase (complex I) of the mitochondrial inner membrane respiratory chain binds a number of mitochondrial matrix NAD-linked dehydrogenases. These include pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase complex, mitochondrial malate dehydrogenase, and beta-hydroxyacyl-CoA dehydrogenase. No binding was detected between complex I and cytosolic malate dehydrogenase, glutamate dehydrogenase, NAD-isocitrate dehydrogenase, lipoamide dehydrogenase, citrate synthase, or fumarase. The dehydrogenases that bound to complex I did not bind to a preparation of complex II and III, nor did they bind to liposomes. The binding of pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase complex, and mitochondrial malate dehydrogenase to complex I is a saturable process. Based upon the amount of binding observed in these in vitro studies, there is enough inner membrane present in the mitochondria to bind the dehydrogenases in the matrix space. The possible metabolic significance of these interactions is discussed.
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PMID:Complex I binds several mitochondrial NAD-coupled dehydrogenases. 643 16

Long-term electrical stimulation (14-28 days) of rabbit fast muscles (tibialis anterior, TA and extensor digitorum longus, EDL) using intermittent high frequency (3 trains per min of 5 s duration at 40 Hz, for 8 h per day) produced changes in enzyme activities similar to those found with continuous stimulation at a frequency occurring in nerves to slow muscles (10 Hz). The activity of citrate synthetase, 3-hydroxyacyl-CoA dehydrogenase and succinate dehydrogenase increased two to 3-fold within 28 days. There was a 4-fold increase in hexokinase whereas phosphofructokinase, pyruvate kinase, lactate dehydrogenase and fructose-1,6-diphosphatase decreased to about 60% of the activity levels in the contralateral unstimulated muscles. Blood flow and oxygen consumption at rest were not changed even after 28 days of stimulation, but were increased during contractions in muscles stimulated at either frequency, the level being twice as high as in control muscles. Glucose uptake was similar to that in control muscles both at rest and during contractions and the output of lactate was similar to that found in control muscles in muscles stimulated at 40 Hz. Muscles stimulated at 10 Hz had smaller lactate output. Thus intermittent stimulation at high frequency (40 Hz) and continuous low frequency (10 Hz) produced similar changes in aerobic metabolism and fuel uptake provided that the total number of stimuli was comparable and that the stimulation was carried out for sufficiently long period.
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PMID:Effects of different patterns of long-term stimulation on blood flow, fuel uptake and enzyme activities in rabbit fast skeletal muscles. 652 41

Eighty-seven male Sprague-Dawley rats (245-300 g) were randomly assigned to one of two experimental groups. The first group consumed a diet high in fat and low in carbohydrate (LCD), whereas the second group ate a normal diet (ND). After either 1 or 5 wk on the diets, rats from each group were killed either before or after an exhausting run on a rodent treadmill (35 m X min-1, 0% grade). The LCD animals ran significantly longer before exhaustion at both week 1 (44.9 +/- 5.1 vs. 41.6 +/- 4.2 min) and week 5 (47.1 +/- 3.6 vs. 35.5 +/- 3.1 min) (P less than 0.05). Adaptations to the LCD included lower muscle and liver glycogen content, decreased rate of glycogen breakdown during exercise, decreased lactate production, and elevated blood ketone levels. In addition to these substrate changes, the LCD caused increased enzyme activities of muscular 3-hydroxyacyl-CoA dehydrogenase (35-110%) and citrate synthase (15-20%). These data indicate that rats exposed to a high-fat diet are capable of prolonged intense exercise in spite of limited glycogen stores. This improved capacity for exercise appears to be partially the result of muscular adaptations to the diet, which apparently increase the ability to oxidize fat and concomitantly spare glycogen.
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PMID:Adaptations to a high-fat diet that increase exercise endurance in male rats. 669 36

Muscle biopsies were obtained from three cyclists and four runners at the end of 10-24 mo of intensive training and after intervals of detraining up to 12 wk. Control samples came from four untrained persons and four former athletes. Macro mixed fiber samples were assayed for lactate dehydrogenase, adenylate kinase, glycogen phosphorylase, citrate synthase, malate dehydrogenase, beta-hydroxyacyl-CoA dehydrogenase, succinate dehydrogenase, beta-hydroxybutyrate dehydrogenase, creatine kinase, hexokinase, 1-phosphofructokinase, fructosebisphosphatase, protein, and total creatine. In the case of three trained persons and two controls, the first six of the enzymes were also measured in individual fibers. Before detraining, enzymes of oxidative metabolism were substantially higher than in controls, and differences in levels between type I and type II fibers were smaller. During detraining, oxidative enzymes were decreased in both fiber types but the type II fibers did not fall to control levels even after 12 wk. Phosphorylase increased with detraining in both fiber types. The same is true for lactate dehydrogenase and adenylate kinase, except in the case of the type I fibers of one individual. Among the other six enzymes (measured in mixed fiber samples), only hexokinase was consistently affected (decreased) by detraining.
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PMID:Effects of detraining on enzymes of energy metabolism in individual human muscle fibers. 682 50

Activities of four catabolic enzymes (citrate synthase, hexokinase, 3-hydroxyacyl-CoA dehydrogenase, and phosphorylase) were measured in the pectoralis muscles of 10 species of South American bats, representing four families. The pattern of enzyme activities in these tissues suggests that these muscles differ qualitatively with other mammalian and avian muscles in two respects. First, the muscles of all 10 bat species were much more highly oriented toward fat metabolism and away from glucose metabolism than in any previously measured skeletal muscle. Second, the species were divided into two major groups with respect to hexokinase activity. Primarily frugivorous species had hexokinase activities about 2-3 times as high as insectivorous species. It is suggested that the weight restrictions of flight limit glycogen storage and thus bias muscle metabolism toward fat. However, the extent to which pectoralis muscles have the capacity for glucose oxidation appears to be dependent on the intake of dietary glucose.
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PMID:Muscle enzyme profile, diet, and flight in South American bats. 706 12

The effect of 6-week endurance training on mitochondrial ATP production rate was investigated in 14 elderly men. Mean age, body weight and height were 63 +/- 6 yr, 75.6 +/- 9.2 kg and 174 +/- 4 cm, respectively. Subjects trained on a Monark cycle ergometer at 79 +/- 8% of their maximal heart rate for 1 h day-1, 4 days week-1. Muscle samples were obtained at rest, before and after endurance training, by a needle biopsy technique and used for determination of mitochondrial ATP production rate in isolated mitochondria and enzyme assays. Endurance training resulted in a significant increase in maximal oxygen uptake (L min-1) (P < 0.01). Citrate synthase activity, a mitochondrial marker enzyme, and hexokinase activity increased significantly (both P < 0.01) in response to training while 3-hydroxyacyl-CoA dehydrogenase and carnitine palmitoyltransferase I activities remained statistically unchanged. A higher mitochondrial ATP production rate was observed after endurance training with the substrate combinations pyruvate+palmitoyl-L-carnitine+L-glutamate+malate (P < 0.01), L-glutamate (P < 0.001), pyruvate+malate (P < 0.05) and palmitoyl-L-carnitine+malate (P < 0.01). The largest increase was obtained with L-glutamate (170%). Significant correlations were observed between the percent increase in citrate synthase activity and those of mitochondrial ATP production rates. It was concluded that the increased mitochondrial ATP production rate of aged human skeletal muscle with training seems mainly to occur through an increased mitochondrial content, and in a way similar to those observed in young men.
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PMID:Mitochondrial ATP production rate in 55 to 73-year-old men: effect of endurance training. 757 22

The activities of three mitochondrial oxidative enzymes (citrate synthase, 3-ketoacid-CoA transferase, beta-hydroxyacyl-CoA dehydrogenase) and Na-K-ATPase were microassayed in isolated segments of the rat proximal convoluted tubule (PCT) and medullary thick ascending limb of the loop of Henle (mTAL). The effects of adrenalectomy (ADX) and ADX plus exogenous glucocorticoids were analyzed. The hormonal replacement was daily injections of dexamethasone (10 micrograms/100 g body weight/24 h) for 5 days. ADX lowered the activity of all oxidative enzymes studies in the mTAL, but not in the PCT and led to a decrease in Na-K-ATPase in both nephron segments. Dexamethasone restored the normal level of oxidative enzymes and Na-K-ATPase in the mTAL and of Na-K-ATPase in the PCT. We conclude that the activities of citrate synthase, 3-ketoacid-CoA transferase and beta-hydroxyacyl-CoA dehydrogenase and of Na-K-ATPase are coordinately regulated in the mTAL and that glucocorticoids are essential for the long-term regulation of these enzyme activities in this nephron segment. In contrast, the activities of mitochondrial oxidative enzymes are not influenced by glucocorticoids in the PCT. This study presents the first evidence for a cell-specific regulation by glucocorticoids of oxidative metabolism in the nephron of adult rat kidney.
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PMID:Effect of glucocorticoids on mitochondrial oxidative enzyme and Na-K-ATPase activities in the rat proximal tubule and thick ascending limb of Henle. 769 38

The purpose of the study was to verify the influence of several weeks of chronic low-frequency electrical stimulation (LFES) on the metabolic profile and functional capacity of human skeletal muscle. Knee extensor muscles (KEM) of eight subjects were electrically stimulated at 8 Hz for 8 h/day and 6 days/wk. Vastus lateralis muscle samples were taken before, after 4 wk, and after 8 wk of LFES, and activities of anaerobic (creatine kinase, phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase) and aerobic-oxidative (citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, cytochrome-c oxidase) enzyme markers were determined. KEM dynamic performance was also assessed before, after 4 wk, and after 8 wk of LFES. Activity levels of anaerobic enzymes were not altered, whereas the activity levels of citrate synthase (29%),3-hydroxyacyl-CoA dehydrogenase (22%), and cytochrome-c oxidase (25%) were significantly increased after 4 wk of LFES but were not further increased after 4 additional wk of LFES. KEM performance was also improved (P < 0.05) but leveled off after 4 wk of LFES. Although significant changes were observed, the results of the present study suggest that the muscle characteristics investigated in the current study have a limited capacity of adaptation in response to this form of chronic LFES.
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PMID:Human skeletal muscle adaptation in response to chronic low-frequency electrical stimulation. 783 13


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