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 metabolic pathways by which the glycogen is utilized by fetal tissues is not well established. In the present study the ontogeny of seven key enzymes involved in glycolysis and the tricarboxylic acid cycle has been established for rabbit fetal lung, heart, and liver. In the fetal lung the activities of phosphofructokinase, pyruvate kinase, lactic dehydrogenase, citrate synthase, and malate dehydrogenase increase from day 21 to 25. Thereafter the levels either drop to day 19 levels or do not change. The isocitrate dehydrogenase activity continues to increase from day 19 of gestation to maximum level on day 31 of gestation. In fetal heart the pattern of activity is similar, but in fetal liver most of the enzymes reach maximum levels earlier and, with the exception of pyruvate kinase, do not show a significant fall in activity near term. The pattern of development of pyruvate dehydrogenase complex is different; maximum activity is observed on day 27 in fetal lung and heart and on day 21 in fetal liver. These results indicate that all three fetal tissues can oxidize glucose. Also, the accumulation of glycogen, particularly in fetal lung, appears to ensure that at specific times during gestation adequate quantities of energy (ATP) and substrates, required for surfactant phospholipid synthesis, are available independent of maternal supply of glucose or during brief episodes of hypoxia.
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PMID:Ontogeny of pyruvate dehydrogenase complex and key enzymes involved in glycolysis and tricarboxylic acid cycle in rabbit fetal lung, heart, and liver. 226 16

1. Maximal activities of some key enzymes of glycolysis, the pentose phosphate pathway, the tricarboxylic acid cycle and glutaminolysis were measured in homogenates from a variety of normal, neoplastic and suppressed cells. 2. The relative activities of hexokinase and 6-phosphofructokinase suggest that, particularly in neoplastic cells, in which the capacity for glucose transport is high, hexokinase could approach saturation in respect to intracellular glucose; consequently, hexokinase and phosphofructokinase could play an important role in the regulation of glycolytic flux in these cells. 3. The activity of pyruvate kinase is considerably higher in tumorigenic cells than in non-tumorigenic cells and higher in metastatic cells than in tumorigenic cells: for non-tumorigenic cells the activities range from 28.4 to 574, for tumorigenic cells from 899 to 1280, and for metastatic cells from 1590 to 1627 nmol/min per mg of protein. 4. The ratio of pyruvate kinase activity to 2 x phosphofructokinase activity is very high in neoplastic cells. The mean is 22.4 for neoplastic cells, whereas for muscle from 60 different animals it is only 3.8. 5. Both citrate synthase and isocitrate dehydrogenase activities are present in non-neoplastic and neoplastic cells, suggesting that the full complement of tricarboxylic-acid-cycle enzymes are present in these latter cells. 6. In neoplastic cells, the activity of glutaminase is similar to or greater than that of hexokinase, which suggests that glutamine may be as important as glucose for energy generation in these cells.
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PMID:Maximum activities of key enzymes of glycolysis, glutaminolysis, pentose phosphate pathway and tricarboxylic acid cycle in normal, neoplastic and suppressed cells. 230 81

Our aim was to delineate the effect(s) of chronic metabolic acidosis on renal TCA-cycle metabolism. Renal tubules isolated from control and chronically acidotic rats were incubated at pH 7.4 with either 2 mM [2,3-13C]pyruvate or [2-13C]acetate. GC-MS and/or 13C-NMR were utilized to monitor the flux of 13C through pyruvate dehydrogenase, pyruvate carboxylase and the TCA-cycle. With either, precursor acidosis was associated with significantly decreased formation of 13C-labelled citrate, malate, aspartate and alanine and increased formation of glucose, lactate and acetyl-CoA as compared with the control. The results indicate that adaptation of renal metabolism to chronic metabolic acidosis is associated with diminished flux through citrate synthetase and concomitantly increased flux through pyruvate carboxylase. The data suggest that depletion of TCA-cycle intermediates and enhanced ammoniagenesis in the kidney of chronically acidotic rats may be regulated at the site of mitochondrial citrate-condensing enzyme.
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PMID:Carbon flux through tricarboxylic acid cycle in rat renal tubules. 230 65

Subjective fatigue was quantified before and 20 days after uncomplicated elective abdominal surgery in 12 patients and compared with changes in heart rate, enzyme activities and skeletal muscle substrates before and after bicycle exercise for 10 min at 65 per cent of patients' preoperative maximum work capacity. Fatigue increased from a mean(s.e.m.) preoperative level of 2.5(0.5) arbitrary units to 4.6(0.5) on postoperative day 20 (P less than 0.01). Body-weight, triceps skinfold thickness and arm circumference decreased postoperatively (P less than 0.02). Postoperative values of muscle enzyme activities indicative of oxidative phosphorylation capacity (citrate synthase and 3-OH-acyl coenzyme A dehydrogenase) were lower than preoperative values (P less than 0.05). Lactate dehydrogenase was unaltered and resting values of muscle glycogen and adenosine triphosphate were higher after operation (P less than 0.05). In response to exercise, heart rate, muscle glucose, glucose-6-phosphate and lactate increased (P less than 0.05), while muscle glycogen and creatine phosphate decreased (P less than 0.05). Increase in postoperative fatigue correlated with the increase in heart rate (P less than 0.05), while no significant correlations were found between fatigue and muscle parameters. Our results suggest that lack of exercise and malnutrition may be of importance in the decrease in work capacity and in fatigue after operation.
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PMID:Skeletal muscle enzyme activities and metabolic substrates during exercise in patients with postoperative fatigue. 232 98

The in vitro metabolism of [1-13C]glucose by Ascaris suum third and fourth-stage larvae was analyzed under different gas phases using 13C nuclear magnetic resonance spectroscopy (13C-NMR). Third-stage larvae (L3) incubated under a gas phase of 85% N2/5% O2/10% CO2 produced trace amounts of [13C]succinate, and molted to fourth-stage larvae (L4) between days 3 and 4 in vitro. However, they appeared to arrest as L3s when incubated under air, or 85% N2/5% O2/10% CO2 in the presence of 2 mM potassium cyanide, or 95% N2/5% CO2. Day 12 L4 (eight days after molting) incubated under 85% N2/5% O2/10% CO2, or 95% N2/5% CO2, or 94% N2/1% O2/5% CO2, produced succinate, acetate, propionate and the branched-chain fatty acids 2-methylvalerate and 2-methylbutyrate by fermentative pathways characteristic of adult body wall muscle. In contrast, when Day 12 L4 were incubated under air, only trace amounts of these acids were detected in the incubation medium. Thus, L4 are capable of synthesizing end-products typical of the adult even in the presence of oxygen, as long as the CO2 tensions are above 5%. As would be predicted, activities of enzymes involved in aerobic metabolism, including citrate synthase, isocitrate dehydrogenase, and cytochrome oxidase, decreased dramatically as L4s underwent the final ecdysis and matured to the adult stage. More importantly, activities of enzymes typical of anaerobic metabolism, including phosphoenolpyruvate carboxykinase and malic enzyme, were substantially elevated in L3s (over their levels in second-stage larvae), and appeared to have reached their adult levels in L3s prior to the third molt, even though L3s still exhibited cyanide sensitivity. Since L3s and L4s have enzymes involved in both aerobic and anaerobic pathways, it is possible that the L3s contain two populations of mitochondria, one which functions aerobically and a second which functions anaerobically.
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PMID:Effect of gas phase on carbohydrate metabolism in Ascaris suum larvae. 250 8

Gill cell suspensions from freshwater (FW)- and seawater (SW)-adapted teleosts were obtained by density gradient centrifugation. The proportion of chloride cells (CCs) in the mixed cell suspensions was estimated using the fluorescent mitochondrial stain, DASPMEI, and ranged from less than 1% (FW-adapted tilapia) to approximately 13% (SW-adapted toadfish). The gill cells displayed relatively high viability based on Trypan Blue exclusion (greater than 75%), lactate dehydrogenase leakage (less than 6.5% h-1), oxygen consumption rates (5-15 mumol g-1 cell wet mass h-1) and ATP levels (1-3 mumol g-1 cell wet mass). There were no obvious differences between the viability of CCs and the other cell types present. An initial comparison of gill oxidative metabolism in SW-adapted tilapia (Oreochromis mossambicus) and toadfish (Opsanus beta) demonstrated that both species oxidized glucose and lactate at substantially greater rates than alanine or oleate. Metabolic rates were significantly higher in toadfish cell suspensions. Kinetic experiments revealed that toadfish gill cells displayed lower values of Km and higher values of Vm for both lactate and glucose, in comparison to tilapia. The elevated metabolism in toadfish gill cells was correlated with increased activities of the oxidative enzyme citrate synthase and Na+/K+-ATPase. The toadfish cell suspensions had a greater proportion of CCs and it is likely that the difference in CC numbers between the two species is the basis for the observed differences in enzyme activities and rates of oxidative metabolism. This idea is supported by the highly significant correlation between Na+/K+-ATPase activity (or CC numbers) and rates of lactate oxidation in gill cell suspensions from FW- and SW-adapted tilapia and toadfish, as well as SW-adapted tilapia chronically treated with cortisol to elevate CC numbers. Although it has been assumed widely that the high metabolic rate of gill tissue reflects, in part, the oxidative demands of the chloride cell, the results of this study provide the first experimental, albeit indirect, evidence for differential rates of metabolism in the various cell types that comprise the gill.
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PMID:Metabolism of isolated fish gill cells: contribution of epithelial chloride cells. 254 65

Aspects of energetic and intermediary metabolism were studied in a colon adenocarcinoma cell line (HT29) by multinuclear magnetic resonance spectroscopy. Experiments were carried out on the HT29-D4 clone, which was isolated by limit dilution techniques. This clone, usually undifferentiated (D4-UD), can be maintained in a differentiated state (D4-D) in a glucose-free medium. Metabolic data were obtained by NMR analysis of perchloric acid extracts from D4-UD and D4-D cells. Phosphorus-31 and proton NMR spectra showed the presence of a large amount of choline and phosphorylcholine in the differentiated state (400% and 200%, respectively, of the levels found in D4-UD cells). Other differences appeared in the content of phosphocreatine (absent in D4-D cells) and myoinositol (absent in D4-UD cells). Carbon-13 spectra were recorded from perchloric acid extracts of cells incubated with [1-13C]-labeled glucose or [2-13C]-labeled acetate. The data indicated that both types of cells metabolize glucose through the glycolytic pathway to give lactate, but only D4-D cells were able to store glucose as glycogen at a very high level. A mathematical analysis of fluxes through the tricarboxylic acid (TCA) cycle was developed on the basis of models derived from previous 14C tracer studies. The model was based on the steady-state labeling of glutamate carbons by the 13C isotope and gave the fraction of labeled acetyl-Coa entering the TCA cycle, and the activity y of anaplerotic reactions relative to the flux through the citrate synthetase reaction. The data indicated that y greater than 0.3 in all cases. Only 15% and 30% of labeled acetyl CoA entered the TCA cycle in D4-UD and D4-D cells, respectively, under labeled glucose incubation: these values were significantly different upon labeled acetate feeding, reaching 55% for D4-UD cells and 85% for D4-D cells. The main result of this study is that the process of differentiation of HT29 cells is correlated with a large increase in the activity of oxidative metabolism.
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PMID:Metabolic changes in undifferentiated and differentiated human colon adenocarcinoma cells studied by multinuclear magnetic resonance spectroscopy. 255 31

When temperature differences are taken into account, turtle brains use glucose at one-sixth the rate reported in rat brains. Na+-K+-ATPase activities are 2- to 2.5-fold higher in rat than in turtle brains. Maximal activities of hexokinase and lactate dehydrogenase are similar, whereas citrate synthase activities are two- to threefold higher in rat than turtle brains at the respective biological temperatures. Voltage-dependent Ca2+ channel densities, when compared between the two species, showed no consistent pattern. These data, along with the threefold differences in density of voltage-dependent Na+ channels reported by Lutz et al., are consistent with the idea that lower rates of channel and pump-mediated Na+ and K+ fluxes result in lower rates of aerobic energy metabolism in turtle brains compared with rat brains.
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PMID:Turtles and rats: a biochemical comparison of anoxia-tolerant and anoxia-sensitive brains. 255 54

The growth and the activity of some enzymes were studied in a Candida lipolytica strain 12a which did not synthesize acids in a medium with glucose under the conditions of nitrogen deficiency. The substrate was not assimilated and cyanide-resistant respiration did not develop in the strain under the conditions of profound nitrogen deficiency. The inability of cells to assimilate glucose at the stationary phase of growth resulted, apparently, from an abrupt decrease of phosphofructokinase and pyruvate dehydrogenase activities in the cells. The activities of pyruvate carboxylase and citrate synthase fell down abruptly at the same time.
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PMID:[Comparative study of Candida lipolytica yeasts with various abilities to produce citrate]. 258 47

The early stages of insulin-dependent diabetes mellitus are characterized by a selective inability to secrete insulin in response to glucose, coupled to a better response to nonnutrient secretagogues. The deficient glucose response may be a result of the autoimmune process directed toward the beta-cells. Interleukin-1 (IL-1) has been suggested to be one possible mediator of immunological damage of the beta-cells. In the present study we characterized the sensitivity of beta-cells to different secretagogues after human recombinant IL-1 beta (rIL-1 beta) exposure. Furthermore, experiments were performed to clarify the biochemical mechanisms behind the defective insulin response observed in these islets. Rat pancreatic islets were isolated and kept in tissue culture (medium RPMI-1640 plus 10% calf serum) for 5 days. The islets were subsequently exposed to 60 pM human recombinant IL-1 beta during 48 h in the same culture conditions as above and examined immediately after IL-1 exposure. The rIL-1 beta-treated islets showed a marked reduction of glucose-stimulated insulin release. Stimulation with arginine plus different glucose concentrations, and leucine plus glutamine partially counteracted the rIL-1 beta-induced reduction of insulin release. The activities of the glycolytic enzymes hexokinase, glucokinase, and glyceraldehyde 3-phosphate dehydrogenase, were similar in control and IL-1-exposed islets. Treatment with IL-1 also did not impair the activities of NADH+- and NADPH+-dependent glutamate dehydrogenase, glutamate-aspartate transaminase, glutamate-alanine transaminase, citrate synthase, and NAD+-linked isocitrate dehydrogenase. The oxidation of D-[6-14C]glucose and L-[U-14C]leucine were decreased by 50% in IL-1-treated islets. Furthermore, there was a significant decrease in the ratios of [2-14C]pyruvate oxidation/[1-14C]pyruvate decarboxylation and L-[U-14C]leucine oxidation/L-[1-14C]leucine decarboxylation, indicating that IL-1 decreases the proportion of generated acetyl-coenzyme-A residues undergoing oxidation. However, in the presence of IL-1 there was a significant increase in L-[U-14C]glutamate oxidation. These combined observations suggest that exposure to IL-1 induces a preferential decrease in glucose-mediated insulin release and mitochondrial glucose metabolism. This mitochondrial dysfunction seems to reflect an impairment in proximal steps of the Krebs cycle. It is conceivable that the IL-1-induced suppression and shift in islet metabolism can be an explanation for the beta-cell insensitivity to glucose observed in the early phases of human and experimental insulin-dependent diabetes mellitus.
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PMID:Differential sensitivity to beta-cell secretagogues in cultured rat pancreatic islets exposed to human interleukin-1 beta. 266 6


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