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)

Men with chronic heart failure (CHF) have alterations in their skeletal muscle that are partially responsible for a decreased exercise tolerance. The purpose of this study was to investigate whether skeletal muscle alterations in women with CHF are similar to those observed in men and if these alterations are related to exercise intolerance. Twenty-five men and thirteen women with CHF performed a maximal exercise test for evaluation of peak oxygen consumption (VO(2)) and resting left ventricular ejection fraction, after which a biopsy of the vastus lateralis was performed. Twenty-one normal subjects (11 women, 10 men) were also studied. The relationship between muscle markers and peak VO(2) was consistent for CHF men and women. When controlling for gender, analysis showed that oxidative enzymes and capillary density are the best predictors of peak VO(2.) These results indicate that aerobically matched CHF men and women have no differences in skeletal muscle biochemistry and histology. However, when CHF groups were separated by peak exercise capacity of 4.5 metabolic equivalents (METs), CHF men with peak VO(2) >4.5 METs had increased citrate synthase and 3-hydroxyacyl-CoA dehydrogenase compared with CHF men with peak VO(2) <4.5 METs. CHF men with a lower peak VO(2) had increased capillary density compared with men with higher peak VO(2). These observations were not reproduced in CHF women. This suggests that differences may exist in how skeletal muscle adapts to decreasing peak VO(2) in patients with CHF.
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PMID:Differences in skeletal muscle between men and women with chronic heart failure. 1113 20

The activity of muscle metabolic enzymes depends on the amount and type of physical training. We examined muscle enzyme adaptation to prolonged training followed by a period of lowered activity in spinal-cord-injured individuals (SCI). Ten SCI [mean age 35 (SEM 2) years, mean body mass 78 (SEM 4) kg, mean time post-injury 12 (SEM 2) years and range of lesion C5-T4] were given 12 months of functional electrical stimulation of an upright cycling motion for 30 min a day, three times a week, followed by 6 months of training once a week. Activities of glycolytic (hexokinase HK, lactate dehydrogenase LDH) and oxidative (citrate synthase CS, 3-hydroxyacyl-CoA dehydrogenase HAD) enzymes were determined in biopsies of the vastus lateralis muscle taken at 0, 3, 6, 12, and 18 months of training. The degree of sympathoadrenergic activity was evaluated from arterial concentrations of catecholamines in response to acute exercise. Training three times a week induced increases (P < 0.05) in HK (150%), LDH (40%), CS (100%), and HAD (70%) activities that reached a plateau after 3 months. Peak oxygen uptake and power output during exercise by electrical stimulation rose continuously over the first 12 months. After reducing the amount of training by two-thirds, HK, LDH and CS activities remained elevated above basal levels (P < 0.05), whereas HAD, power output and maximal oxygen uptake returned to pretraining levels (P > 0.05). It is concluded that most improvements in glycolytic and mitochondrial oxidative enzyme activities induced by long-term training can be maintained in spinal-cord-injured individuals despite a marked reduction in training frequency unrelated to performance or to the degree of sympathoadrenergic impairment.
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PMID:Muscle enzyme adaptation to training and tapering-off in spinal-cord-injured humans. 1141 39

We determined the interaction of diet and training on metabolic adaptations in skeletal muscle and liver, and the consequences of these adaptations for endurance. Eighty rats performed a baseline treadmill run to exhaustion at 16 m min(-1) (RUN1) and were then divided into two groups and given one of two diets: high carbohydrate (CHO) or high fat (FAT). Each dietary group was then divided into one of four subgroups: sedentary control that performed no training (NT); low-intensity running (8 m min(-1); LOW) and two groups who trained at their maximal voluntary running speed without electrical stimulation (28 m min(-1); VMAX). Training volume was identical for LOW and VMAX (1000 m session(-1)) and animals ran 4 days week(-1) for 8 weeks. To assess the interaction of the higher intensity exercise with diet, a second endurance test (RUN2) was undertaken after 6 weeks at either 16 m min(-1) or 28 m min(-1). The NT group ran for a longer duration (increase of 77 %) after FAT than CHO (239 +/- 28 vs. 135 +/- 30 min, P < 0.05) at 16 m min(-1). There were no differences in RUN2 for the LOW group when rats ran at 16 m min(-1) (454 +/- 86 vs. 427 +/- 75 min for CHO and FAT groups, respectively), but rats in the VMAX group fed FAT ran longer than rats fed CHO at 28 m min(-1) (100 +/- 28 vs. 58 +/- 11 min, respectively, P < 0.05). FAT increased the activities of the enzymes citrate synthase, beta-hydroxyacyl-CoA dehydrogenase and carnitine palmitoyl-transferase compared to CHO (P < 0.01), but there was no systematic effect of training. We conclude: (1) there was no additive effect of a high-fat diet on endurance performance when rats performed low-intensity training; (2) running performance at 28 m min(-1) was only enhanced by a high-fat diet after more intense training; (3) diet-induced and training-induced adaptations that increase exercise capacity may be under independent control. Experimental Physiology (2001) 86.4, 499-508.
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PMID:Interaction of diet and training on endurance performance in rats. 1144 29

The fuels used by the hawkmoth Amphion floridensis to power flight are determined by nectar-feeding, with fed moths using primarily carbohydrate and unfed moths using primarily fat. To investigate the metabolic pathways underlying fuel-use flexibility in this species, we measured the maximal activities of several key metabolic enzymes in the flight muscle of fed and unfed individuals, for which metabolic rates and fuel utilization had been previously determined. Hexokinase (HK) and phosphofructokinase (PFK) occur at high activities and, during carbohydrate-fueled flight, are estimated to operate at fractional velocities comparable to those of exclusively carbohydrate-utilizing insects. Females exhibited higher glycolytic enzyme activities than did males, and males regulated PFK activity according to nectar feeding. Although beta-hydroxyacyl-CoA dehydrogenase (HOAD) was found at high activities, carnitine palmitoyl transferase (CPT) was not detectable, suggesting that fatty acids may be utilized via a carnitine-independent pathway during flight. Principal component analysis revealed a tendency for the activities of citrate synthase, HK, PFK, and HOAD to be positively correlated among individuals, as well as a lesser tendency for the activities of glycolytic vs. mitochondrial enzymes to be negatively correlated with each other. However, the principal components did not correlate with variation in either oxygen consumption rate or fuel use in vivo, suggesting that variation in enzyme concentration did not determine differences among individuals in metabolic performance during flight. J. Exp. Zool. 290:108-114, 2001.
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PMID:Fuel use in hawkmoth (Amphion floridensis) flight muscle: enzyme activities and flux rates. 1147 Nov 40

In this study, we examined whether weight loss-induced changes in plasma organochlorine compounds (OC) were associated with those in skeletal muscle markers of glycolytic and oxidative metabolism. Vastus lateralis skeletal muscle enzyme activities and plasma OC (Aroclor 1260, polychlorinated biphenyl 153, p,p'-DDE, beta-hexachlorocyclohexane, and hexachlorobenzene) were measured before and after a weight loss program in 17 men and 20 women. Both sexes showed a similar reduction in body weight (approximately 11 kg) in response to treatment, although men lost significantly more fat mass than women (P < 0.05). Enzymatic markers of glycolysis, phosphofructokinase (PFK) activity, and oxidative metabolism, beta-hydroxyacyl-CoA dehydrogenase (HADH), citrate synthase (CS), and cytochrome c oxidase (COX) activities, remained unchanged after weight loss. A significant increase in plasma OC levels was observed in response to weight loss, an effect that was more pronounced in men. No relationship was observed between changes in OC and those in PFK activity in either sex [-0.31 < r < 0.12, not significant (NS)]. However, the greater the increase in plasma OC levels, the greater the reduction in oxidative enzyme (HADH, CS, COX) activities was in response to weight loss in men (-0.75 < r < -0.50, P < 0.05) but not in women (-0.33 < r < 0.33, NS). These results suggest that the weight loss-induced increase in plasma pollutant levels is likely to be associated with reduced skeletal muscle oxidative metabolism in men but not in women.
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PMID:Weight loss-induced rise in plasma pollutant is associated with reduced skeletal muscle oxidative capacity. 1183 59

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

Owing to its high degree of complexity and plasticity, the cichlid pharyngeal jaw apparatus has often been described as a key evolutionary innovation. The majority of studies investigating pharyngeal muscle behavior and function have done so in the context of feeding. Analysis of enzyme activities (citrate synthase, 3-hydroxyacyl-CoA dehydrogenase and L-lactate dehydrogenase) of pharyngeal muscles in the Lake Malawi cichlid Tramitichromis intermedius revealed differences between pharyngeal jaw muscles and between males and females. Therefore, these muscles have different performance characteristics, resulting in different functional characteristics of the muscles within the complex. Furthermore, the differences between muscles of males and females represent fundamental differences in muscular metabolic processes between sexes. This study is the first to demonstrate that the pharyngeal anatomy is not only used for food processing but is possibly responsible for sound production, in turn influencing sexual selection in cichlid fish.
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PMID:Enzyme activities of pharyngeal jaw musculature in the cichlid Tramitichromis intermedius: implications for sound production in cichlid fishes. 1236 4

In female rats, ovariectomy (OVX) is associated with increased body fat and insulin resistance, and estradiol replacement prevents these alterations. These metabolic changes related to the estrogen-deficient state might be due, in part, to alterations in skeletal muscle substrate metabolism. We tested the hypothesis that estradiol affects the regulation of enzymes involved in substrate oxidation and storage within skeletal muscle. Specifically, we examined enzymes involved in the regulation of glycogen synthesis (glycogen synthase [GS]), glycolysis (phosphofructokinase [PFK]), tricarboxylic acid cycle activity (citrate synthase [CS]), and beta-oxidation (beta-hydroxyacyl-CoA dehydrogenase [beta-HADH]). Twenty-two, female Sprague-Dawley rats (7 to 8 weeks old) were separated into 3 groups: OVX + placebo (P; n = 8), OVX + estradiol (E(2); n = 8), and sham-operated (S; n = 6). Rats from E(2) and P groups were pair-fed to the S group to control for OVX-induced changes in food intake. After 16 days, activities of GS, PFK, CS, and beta-HADH were measured in vastus medialis muscle. GS fractional velocity was significantly lower (P <.05) in P (mean +/- SE; 39.7% +/- 6.2%) compared with both S (61.9% +/- 8.8%) and E(2) (65.8% +/- 8.4%) rats. In addition, E(2) rats (41.4 +/- 2.0) had significantly higher (P <.05) CS activity than P (34.9 +/- 2.0) and S (33.9 +/- 1.4 micromol/min/g) groups. There was no effect of OVX or estradiol replacement on beta-HADH or PFK. Our results suggest that, independent of alterations in food intake, estradiol availability affects the regulation of enzymes involved in nonoxidative glucose disposal (GS) and oxidative metabolism (CS) in skeletal muscle.
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PMID:Effect of ovariectomy and estradiol replacement on skeletal muscle enzyme activity in female rats. 1240 87

To attempt to explain the difference in intrinsic (untrained) endurance running capacity in rats selectively bred over seven generations for either low (LCR) or high running capacity (HCR), the relationship among skeletal muscle capillarity, fiber composition, enzyme activity, and O(2) transport was studied. Ten females from each group [body wt: 228 g (HCR), 247 g (LCR); P = 0.03] were studied at 25 wk of age. Peak normoxic maximum O(2) consumption and muscle O(2) conductance were previously reported to be 12 and 33% higher, respectively, in HCR, despite similar ventilation, arterial O(2) saturation, and a cardiac output that was <10% greater in HCR compared with LCR. Total capillary and fiber number in the medial gastrocnemius were similar in HCR and LCR, but, because fiber area was 37% lower in HCR, the number of capillaries per unit area (or mass) of muscle was higher in HCR by 32% (P < 0.001). A positive correlation (r = 0.92) was seen between capillary density and muscle O(2) conductance. Skeletal muscle enzymes citrate synthase and beta-hydroxyacyl-CoA dehydrogenase were both approximately 40% higher (P < 0.001) in HCR (12.4 +/- 0.7 vs. 8.7 +/- 0.4 and 3.4 +/- 0.2 vs. 2.4 +/- 0.2 mmol. kg(-1). min(-1), respectively), whereas phosphofructokinase was significantly (P = 0.02) lower in HCR (27.8 +/- 1.2 vs. 35.2 +/- 2.5 mmol. kg(-1). min(-1)) and hexokinase was the same (0.65 +/- 0.04 vs. 0.65 +/- 0.03 mmol. kg(-1). min(-1)). Resting muscle ATP, phosphocreatine, and glycogen contents were not different between groups. Taken together, these data suggest that, in rats selectively bred for high-endurance exercise capacity, most of the adaptations for improved O(2) utilization occur peripherally in the skeletal muscles and not in differences at the level of the heart or lung.
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PMID:Selected contribution: skeletal muscle capillarity and enzyme activity in rats selectively bred for running endurance. 1248 71

Endurance exercise training induces mitochondrial biogenesis in skeletal muscle. The peroxisome proliferator activated receptor co-activator 1alpha (PGC-1alpha) has recently been identified as a nuclear factor critical for coordinating the activation of genes required for mitochondrial biogenesis in cell culture and rodent skeletal muscle. To determine whether PGC-1alpha transcription is regulated by acute exercise and exercise training in human skeletal muscle, seven male subjects performed 4 weeks of one-legged knee extensor exercise training. At the end of training, subjects completed 3 h of two-legged knee extensor exercise. Biopsies were obtained from the vastus lateralis muscle of both the untrained and trained legs before exercise and after 0, 2, 6 and 24 h of recovery. Time to exhaustion (2 min maximum resistance), as well as hexokinase II (HKII), citrate synthase and 3-hydroxyacyl-CoA dehydrogenase mRNA, were higher in the trained than the untrained leg prior to exercise. Exercise induced a marked transient increase (P < 0.05) in PGC-1alpha transcription (10- to > 40-fold) and mRNA content (7- to 10-fold), peaking within 2 h after exercise. Activation of PGC-1alpha was greater in the trained leg despite the lower relative workload. Interestingly, exercise did not affect nuclear respiratory factor 1 (NRF-1) mRNA, a gene induced by PGC-1alpha in cell culture. HKII, mitochondrial transcription factor A, peroxisome proliferator activated receptor alpha, and calcineurin Aalpha and Abeta mRNA were elevated (approximately 2- to 6-fold; P < 0.05) at 6 h of recovery in the untrained leg but did not change in the trained leg. The present data demonstrate that exercise induces a dramatic transient increase in PGC-1alpha transcription and mRNA content in human skeletal muscle. Consistent with its role as a transcriptional coactivator, these findings suggest that PGC-1alpha may coordinate the activation of metabolic genes in human muscle in response to exercise.
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PMID:Exercise induces transient transcriptional activation of the PGC-1alpha gene in human skeletal muscle. 1256 9


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