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)

Some enzyme activities and metabolic features of the black Ma melanotic, brown MI melanotic and Ab amelanotic melanomas of hamster were investigated. The activities of hexokinase and phosphofructokinase were similar in all three melanomas, the activity of NAD-dependent glycerol-3-phosphate dehydrogenase was higher in the amelanotic melanoma and that of pyruvate kinase and lactate dehydrogenase were slightly lower in MI than in the other tumors. The activities of citrate synthase, succinate dehydrogenase and malate dehydrogenase were higher in the Ma and MI melanotic melanomas than in the Ab amelanotic melanoma. The rate of labeled CO2 production from 6-14C-glucose, 1,5-14C-citric acid and U-14C-glutamine was about 2 times higher in melanotic melanomas than in amelanotic one, while no significant differences among the three melanomas were found in respect to 1-14C-glucose and U-14C-glycerol-3-phosphate. The production of 14CO2 was much higher from 1-14C-glucose than from 6-14C-glucose in all the melanomas studied. L-DOPA stimulated the production of 14CO2 from 1-14C-glucose much stronger in the Ma and MI melanomas than in the Ab melanoma. In none of the tumors the incorporation from 6-14C-glucose to CO2 was affected by L-DOPA. It is postulated that oxidation of glucose via the pentose phosphate cycle is involved in melanogenesis.
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PMID:Metabolic characterization of three hamster melanoma variants. 406 92

Modifications of enzyme activities (creatine kinase and its B subunit; adenylate kinase; hexokinase; phosphofructokinase; lactate dehydrogenase; malate dehydrogenase, isocitrate dehydrogenase; citrate synthase; acetylcarnitine transferase; beta-hydroxyacetyl-CoA dehydrogenase; cytochrome c oxidase) in gastrocnemius muscle and myocardium were reported after two forms of training with or without administration of anabolic steroid. Endurance training was on a horizontal motor-driven treadmill, 2 km X hr-1, 5 days a week for 0.5 hr per day for 5 weeks. In the case of power endurance training there was a slope of 45 degrees. Enzyme activities in controls and treated guinea pigs, as well as treatment-induced enzyme activity changes are time dependent. Some of these activities correlate linearly with one another; such correlations characterize the effect of adaptation. Endurance training and power endurance training in this study induce similar modifications and seem to differ essentially in the daily work load. The anabolic steroid methandrostenolone (dianabol) induces modifications which training does not bring about but which training at least partially eliminates.
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PMID:Effects of training and methandrostenolone (an anabolic steroid) on energy metabolism in the guinea pig: changes in enzyme activities in gastrocnemius muscle and myocardium. 407 21

Crude extracts of both vegetative cells and glycerol-induced microcysts of Myxococcus xanthus contained the following enzyme activities: phosphofructokinase, phosphoglucoisomerase, fructose-1,6-diphosphatase, fructosediphosphate aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphopyruvate carboxylase, citrate synthase, isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, phosphoglucomutase, and uridine diphosphate glucose pyrophosphorylase. With the exception of isocitrate dehydrogenase, which was present at a fivefold higher concentration in microcysts, all activities in extracts from both types of cells were essentially equal. Hexokinase and pyruvate kinase could not be detected in extracts from either type of cell. Microcysts metabolized acetate at a lower rate than did vegetative cells. Most of this decrease was reflected in a substantial decrease in ability of microcysts to oxidize acetate to CO(2). In addition, microcysts and vegetative cells showed a different distribution of (14)C-label from incorporated acetate.
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PMID:Comparative intermediary metabolism of vegetative cells and microcysts of Myxococcus xanthus. 430 96

1. Transient and steady-state changes caused by acetate utilization were studied in perfused rat heart. The transient period occupied 6min and steady-state changes were followed in a further 6min of perfusion. 2. In control perfusions glucose oxidation accounted for 75% of oxygen utilization; the remaining 25% was assumed to represent oxidation of glyceride fatty acids. With acetate in the steady state, acetate oxidation accounted for 80% of oxygen utilization, which increased by 20%; glucose oxidation was almost totally suppressed. The rate of tricarboxylate-cycle turnover increased by 67% with acetate perfusion. The net yield of ATP in the steady state was not altered by acetate. 3. Acetate oxidation increased muscle concentrations of acetyl-CoA, citrate, isocitrate, 2-oxoglutarate, glutamate, alanine, AMP and glucose 6-phosphate, and lowered those of CoA and aspartate; the concentrations of pyruvate, ATP and ADP showed no detectable change. The times for maximum changes were 1min, acetyl-CoA, CoA, alanine and AMP; 6min, citrate, isocitrate, glutamate and aspartate; 2-4min, 2-oxoglutarate. Malate concentration fell in the first minute and rose to a value somewhat greater than in the control by 6min. There was a transient and rapid rise in glucose 6-phosphate concentration in the first minute superimposed on the slower rise over 6min. 4. Acetate perfusion decreased the output of lactate, the muscle concentration of lactate and the [lactate]/[pyruvate] ratio in perfusion medium and muscle in the first minute; these returned to control values by 6min. 5. During the first minute acetate decreased oxygen consumption and lowered the net yield of ATP by 30% without any significant change in muscle ATP or ADP concentrations. 6. The specific radioactivities of cycle metabolites were measured during and after a 1min pulse of [1-(14)C]acetate delivered in the first and twelfth minutes of acetate perfusion. A model based on the known flow rates and concentrations of cycle metabolites was analysed by computer simulation. The model, which assumed single pools of cycle metabolites, fitted the data well with the inclusion of an isotope-exchange reaction between isocitrate and 2-oxoglutarate+bicarbonate. The exchange was verified by perfusions with [(14)C]bicarbonate. There was no evidence for isotope exchange between citrate and acetyl-CoA or between 2-oxoglutarate and malate. There was rapid isotope equilibration between 2-oxoglutarate and glutamate, but relatively poor isotope equilibration between malate and aspartate. 7. It is concluded that the citrate synthase reaction is displaced from equilibrium in rat heart, that isocitrate dehydrogenase and aconitate hydratase may approximate to equilibrium, that alanine aminotransferase is close to equilibrium, but that aspartate transamination is slow for reasons that have yet to be investigated. 8. The slow rise in citrate concentration as compared with the rapid rise in that of acetyl-CoA is attributed to the slow generation of oxaloacetate by aspartate aminotransferase. 9. It is proposed that the tricarboxylate cycle may operate as two spans: acetyl-CoA-->2-oxoglutarate, controlled by citrate synthase, and 2-oxoglutarate-->oxaloacetate, controlled by 2-oxoglutarate dehydrogenase; a scheme for cycle control during acetate oxidation is outlined. The initiating factors are considered to be changes in acetyl-CoA, CoA and AMP concentrations brought about by acetyl-CoA synthetase. 10. Evidence is presented for a transient inhibition of phosphofructokinase during the first minute of acetate perfusion that was not due to a rise in whole-tissue citrate concentration. The probable importance of metabolite compartmentation is stressed.
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PMID:Control of the tricarboxylate cycle and its interactions with glycolysis during acetate utilization in rat heart. 544 22

Concentration of ([Glc]) and turnover (Ro) of plasma glucose, concentration of free fatty acids in plasma ([FFA]), and concentration of glycogen in muscle and liver were measured in freshly captured summer- and winter-acclimatized American goldfinches (Carduelis tristis). These birds were acutely exposed to one of three thermal regimes: 1) "thermoneutral," 30 degrees C in air, 2) "cold," -15 degrees C in air, and 3) "severe cold," 0 degrees C in 79% He and 21% O2. Additionally, the activities of citrate synthase (CS), phosphofructokinase (PFK), and beta-hydroxyacyl-CoA dehydrogenase (HOAD) were measured in pectoralis and leg muscles of winter and summer birds. Ro for goldfinches at 30 degrees C is unchanged between winter and summer, whereas it is 25% lower at -15 degrees C in winter than in summer birds, even though rates of heat production are similar. Additionally, winter animals depleted muscle glycogen at slower rates than summer individuals when exposed to "cold" or "severe cold." [Glc] and [FFA] for each test regime did not vary between seasons. The activity of the beta-oxidative enzyme HOAD is the pectoralis muscle (the main thermogenic tissue) increases by 50% from summer to winter, but the activities of PFK and CS remain essentially constant. We conclude that the ability to restrict carbohydrate use under cold stress is a component of the winter acclimatization process in the American goldfinch. One mechanism which might foster this ability in the increase in beta-oxidative capacity of the flight muscles, permitting a greater reliance on fatty acids by winter animals during cold-induced thermogenesis.
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PMID:Substrate metabolism in seasonally acclimatized American goldfinches. 621 Nov 5

Eight well-trained middle and long distance male runners added to their regular training program a weekly 20-min treadmill run at a velocity calculated to elicit a blood lactate concentration of 4 mmol X 1-1. VO2 max, the running velocity eliciting 4 mmol X 1-1 blood lactate (VOBLA), and the activities of citrate synthase (CS), phosphofructokinase (PFK), lactate dehydrogenase (LDH) and LDH isozymes in the M. vastus lateralis were determined before and after 14 weeks of this training. Significant increases were observed in VOBLA and the relative fraction of heart-specific LDH, while the activity of PFK and the ratio of PFK/CS decreased after training. The change in VOBLA was negatively correlated to the mean rate of blood lactate accumulation during the last 15 min of the treadmill training runs, and positively correlated to the percentage of slow twitch fibers in the M. vastus lateralis. The data support the hypothesis that a steady state training intensity which approximates VOBLA will increase VOBLA, and will result in measureable local metabolic adaptations in the active skeletal muscles of well-trained runners without a significant change in maximal aerobic power. Muscle fiber type composition may be an indicator of the "trainability" of the musculature.
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PMID:Changes in onset of blood lactate accumulation (OBLA) and muscle enzymes after training at OBLA. 621 7

A mathematical model was used to study the role of various allosteric regulatory mechanisms in the oxidation of glucose and fatty acids by muscle energy metabolism. A large number of such mechanisms were shown to be involved in simultaneous oxidation of both substrates: glycolysis is regulated by the ATP/ADP ratio at the phosphofructokinase (PFK) step; the control over pyruvate dehydrogenase is exercised by the NADHm/NADm+ and CoAsAc/CoAsH ratios as well as by the level of pyruvate; the Krebs cycle is regulated by oxaloacetate and citrate concentrations in the citrate synthase reaction and by the ATP/ADP and NADHm/NADm+ ratios in the isocitrate dehydrogenase reaction. The inhibition of PFK and pyruvate dehydrogenase by excess of CoAsAcyl as well as the inhibition of PFK by citrate are additional equivalent regulatory mechanisms. When glucose alone is oxidized, the levels of citrate, CoAsAcyl, NADHm and CoAsAc decrease drastically within the whole range of physiological ATPase loads; the only regulating factors that remain efficient are the ATP/ADP ratio in glycolysis, the level of pyruvate at the pyruvate dehydrogenase step, the ATP/ADP ratio and the levels of CoAsAc, oxaloacetate and isocitrate in the Krebs cycle.
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PMID:[Mechanisms of the regulation of muscle energy metabolism on oxidation of glucose and fatty acids. A mathematical model]. 621 68

Burn injury is associated with an elevation in total body oxygen consumption, increased hepatic alanine uptake and conversion to glucose, and a negative nitrogen balance. The primary source of the alanine used for gluconeogenesis by the liver and of the nitrogen lost as urea is believed to be from skeletal muscle. Selected muscle regulatory enzymes and pyruvate and oleate oxidation rates were assayed for maximal activity during the postburn period. Male Sprague-Dawley rats that received 50% total body surface scald burns on the dorsum and abdomen were examined for citrate synthase (CS), phosphofructokinase (PFK), and glutamate-pyruvate transaminase (GPT) activity in uninjured muscle at 3, 7, 13, and 20 days postburn, and the ability of muscle to oxidize pyruvate and oleate was measured at 3 and 13 days after injury. Cs, PFK, and GPT activities increased significantly (p less than 0.05) by 13-20 days after injury in the soleus and diaphragm. The epitrochlearis showed no change in CS, but PFK and GPT were elevated within this time frame. The gastrocnemius muscle showed an elevated oleate oxidation rate at 13 days after injury, but no change at 3 days postburn. Pyruvate oxidation rates were unaltered. The results of this study indicate that during the postburn period several metabolic alterations occur in muscle. These adaptations include: (1) elevated CS activity which may be associated with increased oxidative capacity,, (2) increased PFK activity which implies that more substrate is being shuttled through the glycolytic pathway, (3) increased GPT activity which may reflect increased pyruvate conversion to alanine, and (4) increased oleate oxidation rates which demonstrate that muscle is utilizing more fatty acid substrates during the postburn period.
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PMID:Altered muscle metabolism in rats after thermal injury. 621 91

The thermogenic response to catecholamines, i.e., regulatory nonshivering thermogenesis (NST), is significantly reduced in dystrophic hamsters (BIO 14.6) compared with age-matched normals. The possibility that this reduction reflects, in part, lower levels of enzymes in those tissues implicated in NST has been examined by assaying citrate synthase (CS), beta-hydroxyacyl CoA dehydrogenase (HOAD), and phosphofructokinase (PFK), enzymes whose activity reflect the potential flux of substrates through the tricarboxylic acid cycle, beta-oxidation, and glycolysis, respectively. Each enzyme was assayed in brown fat, heart, gastrocnemius, and semitendinosus of 3-mo-old normal (n = 15) and dystrophic (n = 18) hamsters. Brown fat masses from interscapular, cervical, and scapular-axillary regions of dystrophics averaged only 50% those of normals (424 vs. 890 mg). Additionally, markers of aerobic metabolism (CS and HOAD) were significantly reduced in the brown fat from dystrophic animals. (CS activities averaged 59% of normal, whereas HOAD activities averaged 75% of normal). In dystrophic animals CS and HOAD levels were similar to those of normals in cardiac tissue but were significantly elevated in skeletal muscle samples. Tissue PFK activities were reduced only in cardiac tissue of the more affected dystrophics. Thus decreased NST capacity in dystrophic hamsters is accompanied by reduced masses and CS values in brown fat but not by decreases in the aerobic markers in skeletal or cardiac muscle.
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PMID:Metabolic organization of muscle and brown fat of normal and dystrophic hamsters. 621 87

The present study attempts to assess whether the marked seasonal changes in the capacity for shivering thermogenesis in American goldfinches (Carduelis tristis) involve adjustments of metabolic pathways of the pectoralis muscles similar to those observed in mammalian muscle in response to endurance training, i.e., changes favoring increased reliance on fatty acid oxidation and decreased utilization of carbohydrate reserves. Analysis of seasonal changes in enzyme profile of the pectoralis muscle revealed that winter-acclimatized birds have significantly greater (P less than 0.05) activities of phosphorylase, phosphofructokinase, and beta-hydroxy-acyl-CoA dehydrogenase than do birds in other seasons. The activities of citrate synthase and hexokinase do not vary seasonally. These results differ fundamentally from the pattern of changes in enzyme activities associated with endurance adaptation in mammals. Furthermore no seasonal changes were observed in capacities for the oxidation of fatty acids (palmitate and linoleate) or pyruvate in either crude homogenates or isolated mitochondria of goldfinch pectoralis muscles. The oxidation of pyruvate by isolated pectoralis muscle mitochondria was inhibited (greater than 90%) by the oxidation of palmitoyl carnitine at palmitoyl carnitine concentrations as low as 50 microM. These data agree with physiological observations indicating little use of glucose by this tissue during steady-state shivering. However, the extent of this inhibition does not vary seasonally. Therefore the present study fails to document any significant seasonal change in the catabolic pathways of the pectoralis muscle that would link observed seasonal changes in capacity for shivering thermogenesis with a shift in the balance of substrate use by this tissue.
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PMID:Seasonal acclimatization in American goldfinches: the role of the pectoralis muscle. 622 30


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