Journal articles: 'Krebs cycle metabolism'

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Lindsay, Angus, Christopher M. Chamberlain, Bruce A. Witthuhn, Dawn A. Lowe, and James M. Ervasti. "Dystrophinopathy-associated dysfunction of Krebs cycle metabolism." Human Molecular Genetics 28, no. 6 (November 21, 2018): 942–51. http://dx.doi.org/10.1093/hmg/ddy404.

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Shimodahira, Makiko, Shimpei Fujimoto, Eri Mukai, Yasuhiko Nakamura, Yuichi Nishi, Mayumi Sasaki, Yuichi Sato, et al. "Rapamycin impairs metabolism-secretion coupling in rat pancreatic islets by suppressing carbohydrate metabolism." Journal of Endocrinology 204, no. 1 (October 7, 2009): 37–46. http://dx.doi.org/10.1677/joe-09-0216.

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Rapamycin, an immunosuppressant used in human transplantation, impairs β-cell function, but the mechanism is unclear. Chronic (24 h) exposure to rapamycin concentration dependently suppressed 16.7 mM glucose-induced insulin release from islets (1.65±0.06, 30 nM rapamycin versus 2.35±0.11 ng/islet per 30 min, control, n=30, P<0.01) without affecting insulin and DNA contents. Rapamycin also decreased α-ketoisocaproate-induced insulin release, suggesting reduced mitochondrial carbohydrate metabolism. ATP content in the presence of 16.7 mM glucose was significantly reduced in rapamycin-treated islets (13.42±0.47, rapamycin versus 16.04±0.46 pmol/islet, control, n=30, P<0.01). Glucose oxidation, which indicates the velocity of metabolism in the Krebs cycle, was decreased by rapamycin in the presence of 16.7 mM glucose (30.1±2.7, rapamycin versus 42.2±3.3 pmol/islet per 90 min, control, n=9, P<0.01). Immunoblotting revealed that the expression of complex I, III, IV, and V was not affected by rapamycin. Mitochondrial ATP production indicated that the respiratory chain downstream of complex II was not affected, but that carbohydrate metabolism in the Krebs cycle was reduced by rapamycin. Analysis of enzymes in the Krebs cycle revealed that activity of α-ketoglutarate dehydrogenase (KGDH), which catalyzes one of the slowest reactions in the Krebs cycle, was reduced by rapamycin (10.08±0.82, rapamycin versus 13.82±0.84 nmol/mg mitochondrial protein per min, control, n=5, P<0.01). Considered together, these findings indicate that rapamycin suppresses high glucose-induced insulin secretion from pancreatic islets by reducing mitochondrial ATP production through suppression of carbohydrate metabolism in the Krebs cycle, together with reduced KGDH activity.

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Magnusson, I., W. C. Schumann, G. E. Bartsch, V. Chandramouli, K. Kumaran, J. Wahren, and B. R. Landau. "Noninvasive tracing of Krebs cycle metabolism in liver." Journal of Biological Chemistry 266, no. 11 (April 1991): 6975–84. http://dx.doi.org/10.1016/s0021-9258(20)89598-2.

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Ritson, Dougal J. "A cyanosulfidic origin of the Krebs cycle." Science Advances 7, no. 33 (August 2021): eabh3981. http://dx.doi.org/10.1126/sciadv.abh3981.

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The centrality of the Krebs cycle in metabolism has long been interpreted as evidence of its antiquity, and consequently, questions regarding its provenance, and whether it initially functioned as a cycle or not, have received much attention. The present report shows that prebiotic oxidation of α-hydroxy carboxylates can be achieved by UV photolysis of a simple geochemical species (HS−), which leads to α-oxo carboxylates that feature in the Krebs cycle and glyoxylate shunt. Further reaction of these products leads to almost all intermediates of the Krebs cycle proper, succinate semialdehyde bypass, and glyoxylate shunt. Fumarate, the missing Krebs cycle component, and the required α-hydroxy carboxylates can be provided by a highly related hydrogen cyanide chemistry, which also provides precursors for amino acids, nucleotides, and phospholipids.

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Radzikh, Igor, Erica Fatica, Jillian Kodger, Rohan Shah, Ryan Pearce, and Yana I. Sandlers. "Metabolic Outcomes of Anaplerotic Dodecanedioic Acid Supplementation in Very Long Chain Acyl-CoA Dehydrogenase (VLCAD) Deficient Fibroblasts." Metabolites 11, no. 8 (August 13, 2021): 538. http://dx.doi.org/10.3390/metabo11080538.

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Very long-chain acyl-CoA dehydrogenase deficiency (VLCADD, OMIM 609575) is associated with energy deficiency and mitochondrial dysfunction and may lead to rhabdomyolysis and cardiomyopathy. Under physiological conditions, there is a fine balance between the utilization of different carbon nutrients to maintain the Krebs cycle. The maintenance of steady pools of Krebs cycle intermediates is critical formitochondrial energy homeostasis especially in high-energy demanding organs such as muscle and heart. Even-chain dicarboxylic acids are established as alternative energy carbon sources that replenish the Krebs cycle by bypassing a defective β-oxidation pathway. Despite this, even-chain dicarboxylic acids are eliminated in the urine of VLCAD-affected individuals. In this study, we explore dodecanedioic acid (C12; DODA) supplementation and investigate its metabolic effect on Krebs cycle intermediates, glucose uptake, and acylcarnitine profiles in VLCAD-deficient fibroblasts. Our findings indicate that DODA supplementation replenishes the Krebs cycle by increasing the succinate pool, attenuates glycolytic flux, and reduces levels of toxic very long-chain acylcarnitines.

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He, Miao, Mulan Chen, Mingxue Liu, Faqin Dong, Hongfu Wei, and Danni Wang. "Effects and mechanism of riboflavin on the growth of Alcaligenes faecalis under bias conditions." RSC Advances 9, no. 40 (2019): 22957–65. http://dx.doi.org/10.1039/c9ra04066h.

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Costa, C., and E. Galembeck. "THE EVOLUTION OF THE KREBS CYCLE: A PROMISING THEME FOR MEANINGFUL BIOCHEMISTRY LEARNING IN BIOLOGY." Revista de Ensino de Bioquímica 13 (August 24, 2015): 9. http://dx.doi.org/10.16923/reb.v13i2.577.

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INTRODUCTION: Evolution has been recognized as a key concept for biologists. In order to motivate biology undergraduates for contents of central energetic metabolism, we addressed the Krebs cycle structure and functions to an evolutionary view. To this end, we created a study guide which contextualizes the emergence of the cyclic pathway, in light of the prokaryotic influence since early Earth anaerobic condition to oxygen rise in atmosphere. OBJECTIVES: The main goal is to highlight the educational potential of the material whose subject is scarcely covered in biochemistry textbooks. MATERIALS AND METHODS: The study guide is composed by three interrelated sections, the problem (Section 1), designed to arouse curiosity, inform and motivate students; an introductory text (Section 2) about life evolution, including early micro-organisms and Krebs cycle emergence, and questions (Section 3) for debate. The activity consisted on a peer discussion session, with instructors tutoring. The questions were designed to foster exchange of ideas in an ever-increasing level of complexity, and cover subjects from early atmospheric conditions to organization of the metabolism along the subsequent geological ages. RESULTS AND DISCUSSION: We noticed that students were engaged and motivated by the task, especially during group discussion. Based on students’ feedbacks and class observations, we learned that the material raised curiosity and stimulated discussion among peers. It brought a historical and purposeful way of dealing with difficult biochemical concepts. CONCLUSIONS: The whole experience suggests that the study guide was a stimulus for broadening comprehension of the Krebs cycle, reinforcing the evolutionary stance as an important theme for biology and biochemistry understanding. On the other hand, we do not underestimate the fact that approaching Krebs cycle from an evolutionary standpoint is a quite complex discussion for the majority of students. KEYWORDS: Evolution. Krebs cycle. Metabolism learning. Biology. ACKNOWLEDGEMENTS: We thank Capes for financial support.

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Landau, B. R., W. C. Schumann, V. Chandramouli, I. Magnusson, K. Kumaran, and J. Wahren. "14C-labeled propionate metabolism in vivo and estimates of hepatic gluconeogenesis relative to Krebs cycle flux." American Journal of Physiology-Endocrinology and Metabolism 265, no. 4 (October 1, 1993): E636—E647. http://dx.doi.org/10.1152/ajpendo.1993.265.4.e636.

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Purposes of this study were 1) to estimate in humans, using 14C-labeled propionate, the rate of hepatic gluconeogenesis relative to the rate of Krebs cycle flux; 2) to compare those rates with estimates previously made using [3-14C]lactate and [2-14C]acetate; 3) to determine if the amount of ATP required for that rate of gluconeogenesis could be generated in liver, calculated from that rate of Krebs cycle flux and splanchnic balance measurements, previously made, and 4) to test whether hepatic succinyl-CoA is channeled during its metabolism through the Krebs cycle. [2-14C]propionate, [3-14C]-propionate, and [2,3-14C]succinate were given along with phenyl acetate to normal subjects, fasted 60 h. Distributions of 14C were determined in the carbons of blood glucose and of glutamate from excreted phenylacetylglutamine. Corrections to the distributions for 14CO2 fixation were made from the specific activities of urinary urea and the specific activities in glucose, glutamate, and urea previously found on administering [14C]-bicarbonate. Uncertainties in the corrections and in the contributions of pyruvate and Cori cyclings limit the quantitations. The rate of gluconeogenesis appears to be two or more times the rate of Krebs cycle flux and pyruvate's decarboxylation to acetyl-CoA, metabolized in the cycle, less than one-twenty-fifth the rate of its decarboxylation. Such estimates were previously made using [3-14C]lactate. The findings support the use of phenyl acetate to sample hepatic alpha-ketoglutarate. Ratios of specific activities of glucose to glutamate and glucose to urinary urea and expired CO2 indicate succinate's extensive metabolism when presented in trace amounts to liver. Utilizations of the labeled compounds by liver relative to other tissues were in the order succinate = lactate > propionate > acetate. ATP required for gluconeogenesis and urea formation was approximately 40% of the amount of ATP generated in liver. There was no channeling of succinyl-CoA in the Krebs cycle in the hepatic mitochondria.

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Thies, R. S., and L. J. Mandel. "Role of glucose in corneal metabolism." American Journal of Physiology-Cell Physiology 249, no. 5 (November 1, 1985): C409—C416. http://dx.doi.org/10.1152/ajpcell.1985.249.5.c409.

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Glucose catabolism by glycolysis and the Krebs cycle was examined in the isolated rabbit cornea incubated with [6-14C]glucose. The production of [14C]lactate and 14CO2 from this substrate provided minimal values for the fluxes through these pathways since the tissue was in metabolic steady state but not isotopic steady state during the 40-min incubation. The specific activity of lactate under these conditions was one-third of that for [6-14C]glucose, and label dilution by exchange with unlabeled alanine was minimal, suggesting that glycogen degradation was primarily responsible for this dilution of label in the Embden-Meyerhof pathway. In addition, considerable label accumulation was found in glutamate and aspartate. Calculations revealed that these endogenous amino acid pools were not isotopically equilibrated after the incubation period, suggesting that they were responsible for the isotopic nonsteady state by exchange dilution through transaminase reactions with labeled intermediates. An estimate of glucose oxidation by the Krebs cycle, which was corrected for label dilution by exchange, indicated that glucose could account for most of the measured corneal oxygen consumption that was coupled to oxidative phosphorylation. A minor component of this respiration could not be accounted for by glucose or glycogen oxidation. Additional experiments suggested that endogenous fatty acid oxidation was probably also active under these conditions. Finally, reciprocal changes in plasma membrane Na+-K+-ATPase activity induced by ouabain and nystatin were found to concomitantly alter oxygen consumption rates and [14C]lactate production from [6-14C]glucose. These results demonstrated the capacity for regulating glycolysis and the Krebs cycle in response to changing energy demands in the cornea.

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De C. Fonseca, M., C. J. Aguiar, J. A. Da Rocha Franco, R. N. Gingold, and M. F. Leite. "GPR91: EXPANDING THE FRONTIERS OF KREBS CYCLE INTERMEDIATES." Nephrology (Saint-Petersburg) 21, no. 1 (March 3, 2017): 9–18. http://dx.doi.org/10.24884/1561-6274-2017-21-1-9-18.

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Since it was discovered, the citric acid cycle has been known to be central to cell metabolism and energy homeostasis. Mainly found in the mitochondrial matrix, some of the intermediates of the Krebs cycle are also present in the blood stream. Currently, there are several reports that indicate functional roles for Krebs intermediates out of its cycle. Succinate, for instance, acts as an extracellular ligand by binding to a G-protein coupled receptor, known as GPR91, expressed in kidney, liver, heart, retinal cells and possibly many other tissues. Succinate activated GPR91 induces a wide array of physiological and pathological effects. Through GPR91, succinate is involved in functions such as regulation of blood pressure, inhibition of lipolysis in white adipose tissue, development of retinal vascularization, cardiac hypertrophy and activation of stellate hepatic cells by ischemic hepatocytes. Current review is dedicated to discussion of these effects.

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Keller, Markus A., Paul C. Driscoll, Christoph B. Messner, and Markus Ralser. "Primordial Krebs-cycle-like non-enzymatic reactions detected by mass spectrometry and nuclear magnetic resonance." Wellcome Open Research 2 (July 21, 2017): 52. http://dx.doi.org/10.12688/wellcomeopenres.12103.1.

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Background: Metabolism is the process of nutrient uptake and conversion, and executed by the metabolic network. Its evolutionary precursors most likely originated in non-enzymatic chemistry. To be exploitable in a Darwinian process that forms a metabolic pathway, non-enzymatic reactions need to form a chemical network that produces advantage-providing metabolites in a single, life compatible condition. In a hypothesis-generating, large-scale experiment, we recently screened iron and sulfur-rich solutions, and report that upon the formation of sulfate radicals, Krebs cycle intermediates establish metabolism-like non-enzymatic reactivity. A challenge to our results claims that the results obtained by liquid chromatography-selective reaction monitoring (LC-SRM) would not be reproducible by nuclear magnetic resonance spectroscopy (1H-NMR). Methods: This study compared the application of the two techniques to the relevant samples. Results: We detect hundred- to thousand-fold differences in the specific limits of detection between LC-SRM and 1H-NMR to detect Krebs cycle intermediates. Further, the use of 1H-NMR was found generally problematic to characterize early metabolic reactions, as Archean-sediment typical iron concentrations cause paramagnetic signal suppression. Consequently, we selected non-enzymatic Krebs cycle reactions that fall within the determined technical limits. We confirm that these proceed unequivocally as evidenced by both LC-SRM and 1H-NMR. Conclusions: These results strengthen our previous conclusions about the existence of unifying reaction conditions that enables a series of co-occurring metabolism-like non-enzymatic Krebs cycle reactions. We further discuss why constraints applying to metabolism disentangle concentration from importance of any reaction intermediates, and why evolutionary precursors to metabolic pathways must have had much lower metabolite concentrations compared to modern metabolic networks. Research into the chemical origins of life will hence miss out on the chemistry relevant for metabolism if its focus is restricted solely to highly abundant and unreactive metabolites, including when it ignores life-compatibility of the reaction conditions as an essential constraint in enzyme evolution.

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Zong-Chao, Ling, Suad Efendic, Rolf Wibom, Samy M. Abdel-Halim, Claes-Göran Östenson, Bernard R. Landau, and Akhtar Khan. "Glucose Metabolism in Goto-Kakizaki Rat Islets*." Endocrinology 139, no. 6 (June 1, 1998): 2670–75. http://dx.doi.org/10.1210/endo.139.6.6053.

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Abstract Islets from Goto-Kakizaki (GK) rats from our colony, despite marked impairment of glucose-induced insulin release, used glucose and produced CO2 at a rate 3 times that of islets from control Wistar rats. Almost all glucose used was accounted for in CO2 and lactate production. The percentages of glucose carbon used collected in CO2 and lactate were similar for control and GK islets. GK islets also oxidized 40% more acetate and leucine to CO2 than did control islets. The fraction of carbon leaving the Krebs cycle relative to CO2 production was the same in GK and control islets. The capacities of mitochondria from GK islets to generate ATP from glutamate and malate were similar and that to generate ATP from succinate and rotenone was somewhat less from GK islets. The reason for the enhanced utilization of substrates by islets of the GK rat is not apparent. In conclusion, there is no decrease in islet glucose utilization, glucose oxidation, Krebs cycle function, or the electron transport system evident from these measurements to explain the impaired insulin release in islets from GK rats.

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Mishkovsky, Mor, Arnaud Comment, and Rolf Gruetter. "In Vivo Detection of Brain Krebs Cycle Intermediate by Hyperpolarized Magnetic Resonance." Journal of Cerebral Blood Flow & Metabolism 32, no. 12 (September 19, 2012): 2108–13. http://dx.doi.org/10.1038/jcbfm.2012.136.

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The Krebs (or tricarboxylic acid (TCA)) cycle has a central role in the regulation of brain energy regulation and metabolism, yet brain TCA cycle intermediates have never been directly detected in vivo. This study reports the first direct in vivo observation of a TCA cycle intermediate in intact brain, namely, 2-oxoglutarate, a key biomolecule connecting metabolism to neuronal activity. Our observation reveals important information about in vivo biochemical processes hitherto considered undetectable. In particular, it provides direct evidence that transport across the inner mitochondria membrane is rate limiting in the brain. The hyperpolarized magnetic resonance protocol designed for this study opens the way to direct and real-time studies of TCA cycle kinetics.

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Schilling, Oliver, Oliver Frick, Christina Herzberg, Armin Ehrenreich, Elmar Heinzle, Christoph Wittmann, and Jörg Stülke. "Transcriptional and Metabolic Responses of Bacillus subtilis to the Availability of Organic Acids: Transcription Regulation Is Important but Not Sufficient To Account for Metabolic Adaptation." Applied and Environmental Microbiology 73, no. 2 (November 22, 2006): 499–507. http://dx.doi.org/10.1128/aem.02084-06.

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ABSTRACT The soil bacterium Bacillus subtilis can use sugars or organic acids as sources of carbon and energy. These nutrients are metabolized by glycolysis, the pentose phosphate pathway, and the Krebs citric acid cycle. While the response of B. subtilis to the availability of sugars is well understood, much less is known about the changes in metabolism if organic acids feeding into the Krebs cycle are provided. If B. subtilis is supplied with succinate and glutamate in addition to glucose, the cells readjust their metabolism as determined by transcriptome and metabolic flux analyses. The portion of glucose-6-phosphate that feeds into the pentose phosphate pathway is significantly increased in the presence of organic acids. Similarly, important changes were detected at the level of pyruvate and acetyl coenzyme A (acetyl-CoA). In the presence of organic acids, oxaloacetate formation is strongly reduced, whereas the formation of lactate is significantly increased. The alsSD operon required for acetoin formation is strongly induced in the presence of organic acids; however, no acetoin formation was observed. The recently discovered phosphorylation of acetolactate decarboxylase may provide an additional level of control of metabolism. In the presence of organic acids, both types of analyses suggest that acetyl-CoA was catabolized to acetate rather than used for feeding the Krebs cycle. Our results suggest that future work has to concentrate on the posttranslational mechanisms of metabolic regulation.

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ČUPERLOVIĆ-CULF, MIROSLAVA. "THE IMPORTANCE OF INHIBITORS FOR THE SIMULATION OF METABOLIC PROCESSES: IN SILICOZn2+ INHIBITION OF m-ACONITASE FROM ANALYSIS OF GLYCOLYSIS AND KREBS CYCLE KINETIC MODELS." Journal of Bioinformatics and Computational Biology 08, no. 04 (August 2010): 703–15. http://dx.doi.org/10.1142/s0219720010004872.

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Metal ions have a major effect on the metabolic processes in cells either as inhibitors or as integral components of enzymes. The inhibition of enzymes can take place either through the inhibition of gene expression or through inhibition of protein function. A particularly interesting example of the effect of a metal ion on metabolism is the observed inhibition of Krebs cycle and alteration of energy metabolism by zinc (II) cations. In this particular case metal ion inhibition of enzyme is linked to one of the major functions of prostate cells of accumulation and excretion of citrate. Experimental results have shown that increase in concentration of zinc (II) in prostate cells effectively blocks progression of a part of the Krebs cycle leading to change in the concentration of several metabolites with largest effect in the accumulation of citrate. Based on previously reported experimental results, several distinct mechanisms for zinc (II) inhibition of Krebs cycle were proposed. In order to determine the precise mechanism of inhibition in this system, a mathematical model of glycolysis and Krebs cycle was constructed. Three different types of inhibition were analyzed, including competitive and uncompetitive inhibition as well as inhibition through the alteration of the expression level of m-aconitase. The effects of different inhibition models on metabolite concentrations were investigated as a time course simulation of the system of reactions. Several kinetic parameters in the model were optimized in order to best resemble experimental measurements. The simulation shows that only competitive inhibition leads to an agreement with experimental data.

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Bodner, George M. "Metabolism Part II: The tricarboxylic acid (TCA), citric acid, or Krebs cycle." Journal of Chemical Education 63, no. 8 (August 1986): 673. http://dx.doi.org/10.1021/ed063p673.

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Tcherkez, Guillaume, and Graham D. Farquhar. "Viewpoint: Carbon isotope effect predictions for enzymes involved in the primary carbon metabolism of plant leaves." Functional Plant Biology 32, no. 4 (2005): 277. http://dx.doi.org/10.1071/fp04211.

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Carbon isotope effects of enzymes involved in primary carbon metabolism are key parameters in our understanding of plant metabolism. Nevertheless, some of them are poorly known because of the lack of in vitro experimental data on purified enzymes. Some studies have focused on theoretical predictions of isotope effects. Here we show how quantum chemical calculations can be adapted for calculation of isotope effects for the Rubisco-catalysed carboxylation and oxygenation reactions and the citrate synthase reaction. The intrinsic isotope effect of the carboxylation by Rubisco appears to be much smaller than previously thought, being close to the overall isotope effect of the reaction that is, between 25 and 30 per mil. The same applies to the enzyme citrate synthase, that catalyses the first step of the Krebs cycle, with an isotope effect of around 23 per mil. Combined with the isotope effects of equilibrium reactions calculated with β-factors, the Krebs cycle then has an overall isotope effect that depletes organic acids in 13C.

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Atherton, H., M. Schroeder, M. Dodd, D. Ball, J. Griffin, K. Clarke, G. Radda, and D. Tyler. "003 Real-time assessment of Krebs cycle metabolism with hyperpolarised [2-13c]pyruvate." Heart 96, no. 4 (February 1, 2010): e1-e1. http://dx.doi.org/10.1136/hrt.2009.191049c.

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Schroeder, Marie A., Helen J. Atherton, Daniel R. Ball, Mark A. Cole, Lisa C. Heather, Julian L. Griffin, Kieran Clarke, George K. Radda, and Damian J. Tyler. "Real‐time assessment of Krebs cycle metabolism using hyperpolarized C magnetic resonance spectroscopy." FASEB Journal 23, no. 8 (March 27, 2009): 2529–38. http://dx.doi.org/10.1096/fj.09-129171.

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Ugur, Berrak, Huan Bao, Michal Stawarski, Lita R. Duraine, Zhongyuan Zuo, Yong Qi Lin, G. Gregory Neely, Gregory T. Macleod, Edwin R. Chapman, and Hugo J. Bellen. "The Krebs Cycle Enzyme Isocitrate Dehydrogenase 3A Couples Mitochondrial Metabolism to Synaptic Transmission." Cell Reports 21, no. 13 (December 2017): 3794–806. http://dx.doi.org/10.1016/j.celrep.2017.12.005.

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Toyoshima, Shigeki, Fumio Watanabe, Hisako Saido, Ewa H. Pezacka, Donald W. Jacobsens, Kazutaka Miyatake, and Yoshihisa Nakano. "Accumulation of methylmalonic acid caused by vitamin B12-deficiency disrupts normal cellular metabolism in rat liver." British Journal of Nutrition 75, no. 6 (June 1996): 929–38. http://dx.doi.org/10.1079/bjn19960198.

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To clarify the relationship between intracellular concentrations of methylmalonic acid and metabolic and growth inhibition in vitamin B12-deficient rats, hepatic methylmalonic acidlevels were assayed and inhibition of glucose and glutamic acid metabolism by methylmalonic acid was studied in isolated hepatocytes. Vitamin B12-deficient rats (14 weeks old) excreted more urinary methylmalonic acid and had lower body weights than the control rats. Hepatic methylmalonic acid levels (3·6 (SD 1·30)–5·3 (SD 0·51) µmol/g tissue; 7·9 (SD 2·90)–11·8 (SD 1·14) mM) were increased and correlated with the extent of the growth retardation during vitamin B12-deficiency. Isolated hepatocytes and mitochondria from normally fed rats were labelled with [14C(U)]glucose and [14C(U)]glutamic acid respectively, in the presence or absence of 5mM-methylmalonic acid. Although methylmalonic acid did not affect the incorporation of14C into protein and organic acid fractions in the hepatocytes, it inhibited14CO2formation (an index of glucose oxidation by the Krebs cycle) by 25% and incorporation of14C into the amino acid fractionby 30%. In the mitochondria, methylmalonic acid inhibited14CO2, formation (indicating glutamic acid oxidation by the Krebs cycle) by 70%, but not the incorporation of14C into the protein fraction. The incorporation of14C into the organic acid fraction was significantly stimulated by the addition of methylmalonic acid. These results indicate that the unusual accumulation of methylmalonic acid caused by vitamin B12-deficiency disrupts normal glucose and glutamic acid metabolism in rat liver, probably by inhibiting the Krebs cycle.

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Rieger, D., NM Loskutoff, and KJ Betteridge. "Developmentally related changes in the uptake and metabolism of glucose, glutamine and pyruvate by cattle embryos produced in vitro." Reproduction, Fertility and Development 4, no. 5 (1992): 547. http://dx.doi.org/10.1071/rd9920547.

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The metabolism of, and retention of radioactivity from, radiolabelled glucose, glutamine and pyruvate were measured in individual cattle embryos produced in vitro from the 2-cell to hatched blastocyst stage. Uptake was defined as the numeric sum of metabolism and retention of radiolabel. Glucose metabolism increased significantly between the 8- and 16-cell stages, but was accompanied by a much larger increase in glucose uptake. Consequently, the proportion of glucose uptake that was metabolized through the pentose-phosphate and Embden-Meyerhof pathways reached a minimum at those stages. From the compacted morula stage onward, the calculated uptake of [14C]glucose was only 25 to 33% of that calculated for [5-3H]glucose. This suggests that 66 to 75% of glucose carbon leaves the embryo, after metabolism to phosphoenolpyruvate, in some form other than CO2. Little or no glucose metabolism by the Krebs cycle could be detected at any stage. Both glutamine and pyruvate metabolism were relatively high at the 2- and 4-cell stages, declined to a minimum at the compacted morula stage and then increased with blastulation. Glutamine metabolism continued to increase with expansion and hatching of the blastocyst, but pyruvate metabolism did not. This suggest that, relative to the activity of the pathway from pyruvate to 2-oxoglutarate, the activity of the 2-oxoglutarate-to-oxaloacetate segment of the Krebs cycle is of increasing significance during expansion and hatching of the cattle blastocyst.

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Tahmasbi, A. M., H. Galbraith, and J. R. Scaife. "The influence of biotin on viability, pyruvate carboxylase activity and the response to malate concentration in vitro by isolated secondary hair follicles of the Angora goat." Proceedings of the British Society of Animal Science 1999 (1999): 158. http://dx.doi.org/10.1017/s1752756200003136.

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Biotin is a prosthetic group for a number of enzymes involved in carboxylation reactions. Biotin deficiency has been associated with poor growth of integumental tissues by currently unknown mechanisms. Pyruvate carboxylase is a biotin-dependent enzyme which has an important anaplerotic role in intermediary metabolism, catalysing the formation of oxaloacetate from pyruvate and bicarbonate. It thus provides oxaloacetate for gluconeogenesis and replenishes Krebs cycle intermediates. Biotin deficiency may reduce pyruvate carboxylase activity and so oxaloacetate production. Malate is a Krebs cycle intermediate which can convert to oxaloacetate and reduce demand for oxaloacetate generated by pyruvate carboxylase. The aims of the study were to determine (a) the effect of biotin supplementation of the medium on hair follicle viability and pyruvate carboxylase activity and (b) the response to supplementation of the culture medium with malate.

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Swenson, Erik R. "Does Aerobic Respiration Produce Carbon Dioxide or Hydrogen Ion and Bicarbonate?" Anesthesiology 128, no. 5 (May 1, 2018): 873–79. http://dx.doi.org/10.1097/aln.0000000000002125.

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Abstract Maintenance of intracellular pH is critical for clinical homeostasis. The metabolism of glucose, fatty acids, and amino acids yielding the generation of adenosine triphosphate in the mitochondria is accompanied by the production of acid in the Krebs cycle. Both the nature of this acidosis and the mechanism of its disposal have been argued by two investigators with a long-abiding interest in acid–base physiology. They offer different interpretations and views of the molecular mechanism of this intracellular pH regulation during normal metabolism. Dr. John Severinghaus has posited that hydrogen ion and bicarbonate are the direct end products in the Krebs cycle. In the late 1960s, he showed in brain and brain homogenate experiments that acetazolamide, a carbonic anhydrase inhibitor, reduces intracellular pH. This led him to conclude that hydrogen ion and bicarbonate are the end products, and the role of intracellular carbonic anhydrase is to rapidly generate diffusible carbon dioxide to minimize acidosis. Dr. Erik Swenson posits that carbon dioxide is a direct end product in the Krebs cycle, a more widely accepted view, and that acetazolamide prevents rapid intracellular bicarbonate formation, which can then codiffuse with carbon dioxide to the cell surface and there be reconverted for exit from the cell. Loss of this “facilitated diffusion of carbon dioxide” leads to intracellular acidosis as the still appreciable uncatalyzed rate of carbon dioxide hydration generates more protons. This review summarizes the available evidence and determines that resolution of this question will require more sophisticated measurements of intracellular pH with faster temporal resolution.

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Zalewski, Kazimierz. "The metabolism of aged seeds. The involvement of the pentose phosphate pathway in respiration in germinating rye grains of various ages." Acta Societatis Botanicorum Poloniae 61, no. 2 (2014): 167–75. http://dx.doi.org/10.5586/asbp.1992.014.

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Winter rye grains from different harvest years (having distinctly different viabilities) were studied in terms of germination, total dehydrogenase activity and growth analysis. Reduction of seed vigor and viability was accompanied by a decrease in the intensity of embryo respiration during germination. The use of (1-14C) glucose and (6-14C) glucose showed that germinating rye embryos catabolize glucose through glycolysis, Krebs cycle and the pentose phosphate pathway. It was also shown that the C6/C1 ratio in respiring embryos initially increased during the first 48 hours of germination, then dropped, which suggests a mounting contribution of the PP pathway to the overall cotabolism. The oxidation of glucose in, embryos from the most deteriorated grains proceeded through glycolysis and Krebs cycle only.

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Tatarkova, Zuzana, Jeroen H. F. de Baaij, Marian Grendar, Jörg R. Aschenbach, Peter Racay, Caro Bos, Gerhard Sponder, et al. "Dietary Mg2+ Intake and the Na+/Mg2+ Exchanger SLC41A1 Influence Components of Mitochondrial Energetics in Murine Cardiomyocytes." International Journal of Molecular Sciences 21, no. 21 (November 3, 2020): 8221. http://dx.doi.org/10.3390/ijms21218221.

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Cardiomyocytes are among the most energy-intensive cell types. Interplay between the components of cellular magnesium (Mg) homeostasis and energy metabolism in cardiomyocytes is poorly understood. We have investigated the effects of dietary Mg content and presence/functionality of the Na+/Mg2+ exchanger SLC41A1 on enzymatic functions of selected constituents of the Krebs cycle and complexes of the electron transport chain (ETC). The activities of aconitate hydratase (ACON), isocitrate dehydrogenase (ICDH), α-ketoglutarate dehydrogenase (KGDH), and ETC complexes CI–CV have been determined in vitro in mitochondria isolated from hearts of wild-type (WT) and Slc41a1−/− mice fed a diet with either normal or low Mg content. Our data demonstrate that both, the type of Mg diet and the Slc41a1 genotype largely impact on the activities of enzymes of the Krebs cycle and ETC. Moreover, a compensatory effect of Slc41a1−/− genotype on the effect of low Mg diet on activities of the tested Krebs cycle enzymes has been identified. A machine-learning analysis identified activities of ICDH, CI, CIV, and CV as common predictors of the type of Mg diet and of CII as suitable predictor of Slc41a1 genotype. Thus, our data delineate the effect of dietary Mg content and of SLC41A1 functionality on the energy-production in cardiac mitochondria.

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Fatica, Erica M., Gina A. DeLeonibus, Alisha House, Jillian V. Kodger, Ryan W. Pearce, Rohan R. Shah, Liraz Levi, and Yana Sandlers. "Barth Syndrome: Exploring Cardiac Metabolism with Induced Pluripotent Stem Cell-Derived Cardiomyocytes." Metabolites 9, no. 12 (December 17, 2019): 306. http://dx.doi.org/10.3390/metabo9120306.

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Barth syndrome (BTHS) is an X-linked recessive multisystem disorder caused by mutations in the TAZ gene (TAZ, G 4.5, OMIM 300394) that encodes for the acyltransferase tafazzin. This protein is highly expressed in the heart and plays a significant role in cardiolipin biosynthesis. Heart disease is the major clinical manifestation of BTHS with a high incidence in early life. Although the genetic basis of BTHS and tetralinoleoyl cardiolipin deficiency in BTHS-affected individuals are well-established, downstream metabolic changes in cardiac metabolism are still uncovered. Our study aimed to characterize TAZ-induced metabolic perturbations in the heart. Control (PGP1-TAZWT) and TAZ mutant (PGP1-TAZ517delG) iPS-CM were incubated with 13C6-glucose and 13C5-glutamine and incorporation of 13C into downstream Krebs cycle intermediates was traced. Our data reveal that TAZ517delG induces accumulation of cellular long chain acylcarnitines and overexpression of fatty acid binding protein (FABP4). We also demonstrate that TAZ517delG induces metabolic alterations in pathways related to energy production as reflected by high glucose uptake, an increase in glycolytic lactate production and a decrease in palmitate uptake. Moreover, despite mitochondrial dysfunction, in the absence of glucose and fatty acids, TAZ517delG-iPS-CM can use glutamine as a carbon source to replenish the Krebs cycle.

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Davis, M. Benjamin, and Helga Guderley. "Energy Metabolism in the Locomotor Muscles of the Common Murre (Uria aalge) and the Atlantic Puffin (Fratercula arctica)." Auk 104, no. 4 (October 1, 1987): 733–39. http://dx.doi.org/10.1093/auk/104.4.733.

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Abstract To compare the metabolic systems that support the combination of flying and diving with those used to support burst flying and sustained flying, myoglobin concentrations and maximum enzyme activities were determined for selected enzymes of glycolysis, the Krebs cycle, and amino acid metabolism in the pectoral, supracoracoideus, and sartorius muscles of the Common Murre (Uria aalge), Atlantic Puffin (Fratercula arctica), Rock Dove (Columba livia; hereafter "pigeon"), and Ring-necked Pheasant (Phasianus colchicus). Glycolytic enzyme levels in the flight muscles were lower in the murre and the puffin than in the pheasant, while both glycolytic and Krebs-cycle enzyme levels resembled those in the pigeon. We believe puffins and murres do not rely extensively on anaerobic glycolysis during diving. In concordance with a role in oxygen storage for diving, the levels of myoglobin in the flight muscles of murres and puffins were higher than those in pigeons or pheasants. They were lower than published values for penguins, however. In contrast to the trends for pigeon and pheasant muscles, the alcid sartorius muscles had a considerably lower aerobic orientation than the flight muscles.

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van Grinsven, Koen W. A., Jan Van Den Abbeele, Peter Van den Bossche, Jaap J. van Hellemond, and Aloysius G. M. Tielens. "Adaptations in the Glucose Metabolism of Procyclic Trypanosoma brucei Isolates from Tsetse Flies and during Differentiation of Bloodstream Forms." Eukaryotic Cell 8, no. 8 (June 19, 2009): 1307–11. http://dx.doi.org/10.1128/ec.00091-09.

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ABSTRACT Procyclic forms of Trypanosoma brucei isolated from the midguts of infected tsetse flies, or freshly transformed from a strain that is close to field isolates, do not use a complete Krebs cycle. Furthermore, short stumpy bloodstream forms produce acetate and are apparently metabolically preadapted to adequate functioning in the tsetse fly.

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Takeuchi, Kasumi, Patrick Kiefer, Cornelia Reimmann, Christoph Keel, Christophe Dubuis, Joëlle Rolli, Julia A. Vorholt, and Dieter Haas. "Small RNA-dependent Expression of Secondary Metabolism Is Controlled by Krebs Cycle Function inPseudomonas fluorescens." Journal of Biological Chemistry 284, no. 50 (October 19, 2009): 34976–85. http://dx.doi.org/10.1074/jbc.m109.052571.

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Rudzite, Vera, Edite Jurika, Gabriele Baier-Bitterlich, Bernhard Widner, Gilbert Reibnegger, and Dietmar Fuchs. "Pteridines and Lipid Metabolism." Pteridines 9, no. 2 (May 1998): 103–12. http://dx.doi.org/10.1515/pteridines.1998.9.2.103.

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Summary The effect of 9 different pteridines on fatty acid incorporation into phospholipids as well as on cholesterol and phospholipid content was compared in vitro using rat liver homogenate, Krebs-Ringer phosphate buffer containing 0.3 % albumin (pH=7.4), fatty acid mixture and glycerol. D-neopterin (5-30 pmol/g) induced an increase of saturated, a decrease of unsaturated fatty acids incorporation into phospholipids and elevated the cholesterol content in samples. The phospholipid amount in samples remained unchanged. Sepiapterin, 7,8-dihydrobiopterin, 5,6,7,8-tetrahydrobiopterin, biopterin, monapterin and 7,8-dihydroneopterin addition to samples induced an inverse relationship: a decrease of saturated, an increase of unsaturated fatty acid, especially arachidonic acid, incorporation into phospholipids and the decrease of cholesterol content in samples. The phospholipid amount in samples remained unchanged or increased. Lipid metabolism was not altered after addition of xanthopterin and isoxanthopterin to samples. It was suggested that neopterin decreased membrane fluidity, prevented cell cycle, induced cell dystrophy and apoptosis, and promoted the cholesterol precipitation while tetrahydrobiopterin, its precursors, biopterin, monapterin and dihydroneopterin increased membrane fluidity, stimulated cell cycle, prevented cholesterol precipitation. The data point to a potential role of increased neopterin concentrations in vivo to support atherosclerosis development and progression whereas the other pteridines may have a protective effect. Moreover, these pteridines can also promote cell transformation.

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Yuneva, Mariia, Nicola Zamboni, Peter Oefner, Ravi Sachidanandam, and Yuri Lazebnik. "Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cells." Journal of Cell Biology 178, no. 1 (July 2, 2007): 93–105. http://dx.doi.org/10.1083/jcb.200703099.

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The idea that conversion of glucose to ATP is an attractive target for cancer therapy has been supported in part by the observation that glucose deprivation induces apoptosis in rodent cells transduced with the proto-oncogene MYC, but not in the parental line. Here, we found that depletion of glucose killed normal human cells irrespective of induced MYC activity and by a mechanism different from apoptosis. However, depletion of glutamine, another major nutrient consumed by cancer cells, induced apoptosis depending on MYC activity. This apoptosis was preceded by depletion of the Krebs cycle intermediates, was prevented by two Krebs cycle substrates, but was unrelated to ATP synthesis or several other reported consequences of glutamine starvation. Our results suggest that the fate of normal human cells should be considered in evaluating nutrient deprivation as a strategy for cancer therapy, and that understanding how glutamine metabolism is linked to cell viability might provide new approaches for treatment of cancer.

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Barosa, Cristina, Rogério T. Ribeiro, Rita Andrade, João F. Raposo, and John G. Jones. "Effects of Meal Fructose/Glucose Composition on Postprandial Glucose Appearance and Hepatic Glycogen Synthesis in Healthy Subjects." Journal of Clinical Medicine 10, no. 4 (February 5, 2021): 596. http://dx.doi.org/10.3390/jcm10040596.

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Dietary fructose overshadows glucose in promoting metabolic complications. Intestinal fructose metabolism (IFM) protects against these effects in rodents, by favoring gluconeogenesis, but the extent of IFM in humans is not known. We therefore aimed to infer the extent of IFM by comparing the contribution of dietary fructose to systemic glucose and hepatic glycogen appearance postprandially. Twelve fasting healthy subjects ingested two protein meals in random order, one supplemented with 50 g 5/95 fructose/glucose (LF) and the other with 50 g 55/45 fructose/glucose (HF). Sources of postprandial plasma glucose appearance and hepatic glycogen synthesis were determined with deuterated water. Plasma glucose excursions, as well as pre- and post-meal insulin, c-peptide, and triglyceride levels were nearly identical for both meals. The total gluconeogenic contribution to plasma glucose appearance was significantly higher for HF versus LF (65 ± 2% vs. 34 ± 3%, p < 0.001). For HF, Krebs cycle anaplerosis accounted for two-thirds of total gluconeogenesis (43 ± 2%) with one-third from Triose-P sources (22 ± 1%). With LF, three-quarters of the total gluconeogenic contribution originated via Krebs cycle anaplerosis (26 ± 2%) with one-quarter from Triose-P sources (9 ± 2%). HF and LF gave similar direct and indirect pathway contributions to hepatic glycogen synthesis. Increasing the fructose/glucose ratio had significant effects on glucose appearance sources but no effects on hepatic glycogen synthesis sources, consistent with extensive IFM. The majority of fructose carbons were converted to glucose via the Krebs cycle.

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Duvert, Michel, Lucienne Gourdoux, and Robert Moreau. "Cytochemical and physiological studies of the energetic metabolism and osmotrophy in Sagitta friderici (chaetognath)." Journal of the Marine Biological Association of the United Kingdom 80, no. 5 (October 2000): 885–90. http://dx.doi.org/10.1017/s0025315400002861.

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Different glucidic labelled compounds were used for carbohydrate metabolism exploration, tissular glycogen storage localization and amino acid uptake response to osmotic variation in the adult of Sagitta friderici.After [1-14C] glucose or [6-14C] glucose (osmotrophic) assimilation, the relative activity of the different metabolic pathways (glycolysis–citric acid cycle and pentose cycle) have been estimated by means of a micro-radiorespirometric method. The kinetics of expired 14CO2 showed that adult Sagitta mainly used the glycolytic–Krebs cycle rather than the pentose cycle in glucose catabolism.After 2-deoxy-D-[1-14C] glucose (osmotrophic) assimilation, tissular glycogen storages were localized. It was shown that glycogen deposits are abundant in several tissues except the locomotor muscles, which probably represent the main glucose consumers in these very active animals. The problem of glucose transport from the storage localizations to the sites of utilization has been discussed.The L-3H-leucine uptake variations into the Sagitta body after an osmotic shock have been estimated.

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Malaisse, W. J., L. Ladrière, T. M. Zhang, I. Verbruggen, and R. Willem. "Enzyme-to-enzyme channelling of symmetric Krebs cycle intermediates in pancreatic islet cells." Diabetologia 39, no. 8 (August 1996): 990–92. http://dx.doi.org/10.1007/bf00403920.

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Malaisse, W. J., L. Ladri�re, T. M. Zhang, I. Verbruggen, and R. Willem. "Enzyme-to-enzyme channelling of symmetric Krebs cycle intermediates in pancreatic islet cells." Diabetologia 39, no. 8 (July 1, 1996): 990–92. http://dx.doi.org/10.1007/s001250050542.

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37

Ostrenko, K. S., V. P. Galochkina, V. О. Lemiasheuski, A. V. Agafonova, A. N. Ovcharova, N. V. Belova, and I. V. Kutin. "Correlation of dicarboxylic acid cycle with tricarboxylic acid cycle in highly productive pigs." Proceedings of the National Academy of Sciences of Belarus. Agrarian Series 58, no. 2 (May 12, 2020): 215–25. http://dx.doi.org/10.29235/1817-7204-2020-58-2-215-225.

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The paper is the fundamental beginning of research series aimed at understanding the processes associated with high performance in higher animals. The research aim is to study correlation of dicarboxylic acid cycle with tricarboxylic acid cycle with establishment of activity and dislocation of enzymes, confirming the hypothesis of availability and active metabolic participation of peroxisome in highly productive animals. Research was conducted on the basis of the VNIIFBiP animal vivarium in 2019 with a group of piglets of the Irish Landrace breed (n = 10). After slaughter at the age of 210 days, the nuclear (with large tissue particles), mitochondrial and postmitochondrial fractions of the liver were studied with assessment of succinate dehydrogenase and activity of other dehydrogenes of the Krebs cycle. It was found that peroxisomes act as universal agents of communication and cooperation, and microtelets are able to generate various chemical signals that carry information, to control and arrange a number of mechanisms in the metabolic processes in the body. Despite the fact that the Krebs cycle dehydrogenases are considered mitochondrial enzymes, the experiment showed an increase in activity of priruvate dehydrogenase (P > 0.1), isocitrate dehydrogenase (0.1 > P > 0.05) and malate dehydrogenase (0.1 > P > 0.05), which, when comparing the mitochondrial and postmitochondrial fractions, indicates a higher activity of peroxisomal fractions. The peroxisome localization place is the postmitochondrial fraction, and the lower layer contains larger peroxisomes to a greater extent, while the upper layer contains smaller ones. It was found that indicator enzymes of glyoxylate cycle isocitratliase and malate synthase exhibit catalytic activity in the peroxisomal fraction of liver of highly productive pigs. The obtained data on functioning of key glyoxylate cycle enzymes and their intracellular compartmentalization in highly productive pigs allow learning more about the specifics of metabolism and its regulation processes. Application of this knowledge in practice opens up prospects for rationalizing the production of livestock products of increased quantity, improved quality with less feed, labor and financial resources spent.

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Walker, Robert P., Zhi-Hui Chen, and Franco Famiani. "Gluconeogenesis in Plants: A Key Interface between Organic Acid/Amino Acid/Lipid and Sugar Metabolism." Molecules 26, no. 17 (August 24, 2021): 5129. http://dx.doi.org/10.3390/molecules26175129.

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Gluconeogenesis is a key interface between organic acid/amino acid/lipid and sugar metabolism. The aims of this article are four-fold. First, to provide a concise overview of plant gluconeogenesis. Second, to emphasise the widespread occurrence of gluconeogenesis and its utilisation in diverse processes. Third, to stress the importance of the vacuolar storage and release of Krebs cycle acids/nitrogenous compounds, and of the role of gluconeogenesis and malic enzyme in this process. Fourth, to outline the contribution of fine control of enzyme activity to the coordinate-regulation of gluconeogenesis and malate metabolism, and the importance of cytosolic pH in this.

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39

Lee, Hae-In, Chan Seo, Man-Jeong Paik, and Mi-Kyung Lee. "Monitoring of Energy Metabolism by Organic Acid Profiling Analysis in Plasma of Type 2 Diabetic Mice." Current Metabolomics and Systems Biology 7, no. 1 (September 6, 2020): 42–50. http://dx.doi.org/10.2174/2666338407666190828155646.

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Objective:: This study was conducted to investigate energy metabolism based on changes in organic acids in diabetes and to establish a correlation between metabolites or bone microarchitecture and the glucose index in type 2 diabetic mice. Method:: Seven-week-old male C57BL/6 mice were randomly divided into a non-diabetic group and a diabetic group. The diabetic group was fed a high-fat diet (HFD) that induced insulin resistance for 5 weeks. Afterwards, diabetes was induced by a single streptozotocin injection. Both the groups were fed a normal diet and HFD diet for 9 weeks. Results:: The fasting blood glucose level glycosylated hemoglobin (HbA1c) significantly increased in diabetic mice. Bone-alkaline phosphatase activity decreased in the diabetic group. Diabetes increased the levels of ketone bodies, including 3-hydroxybutyric, acetoacetic and butyric acid, whereas it decreased Krebs cycle components, including succinic acid and malic acid, as well as levels of glycolytic products, including lactic acid. Diabetes also induced a shortage of trabecular bone mineral density (BMD) by the regulation of trabecular morphometric parameters in the femur and tibia. Correlation analysis indicated that BMD, Krebs cycle components and lactic acid levels were negatively correlated with HbA1c, whereas ketone bodies were positively correlated with HbA1c. Conclusion: : This research suggested that uncontrolled HbA1c can affect bone loss, production of ketone bodies and utilization of glucose metabolites for energy production in type 2 diabetes.

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Perumal, Selvanathan Saravana, Palanivelu Shanthi, and Panchanadham Sachdanandam. "Energy-modulating vitamins – a new combinatorial therapy prevents cancer cachexia in rat mammary carcinoma." British Journal of Nutrition 93, no. 6 (June 2005): 901–9. http://dx.doi.org/10.1079/bjn20051439.

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Mitochondria are the major intracellular organelles producing ATP molecules via the electron transport chain. Cancer cells have a deviant energy metabolism, and a high rate of glycolysis is related to a high degree of dedifferentiation and proliferation. The overall net ATP production is diminished with cancer, which ultimately leads to cancer cachexia. The present study was designed to investigate the altered energy metabolism in cancer cells and to enhance ATP production in the normal host cell metabolism by enhancing the activities of mitochondrial enzymes, using energy-modulating vitamins, and thus prevent cancer cachexia. Female Sprague–Dawley rats were selected for the experimental study. Mammary carcinoma was induced by the oral administration of 7,12-dimethylbenz[a]anthracene (25 mg/kg body weight), and treatment was started by the oral administration of the energy-modulating vitamins riboflavin (45 mg/kg body weight per d), niacin (100 mg/kg body weight per d) and coenzyme Q10(40 mg/kg body weight per d) for 28 d. Mitochondria were isolated from the mammary gland and liver of all four groups, and the Krebs cycle and oxidative phosphorylation enzymes were assayed. In mammary carcinoma-bearing animals, the activities of the Krebs cycle and oxidative phosphorylation enzymes were significantly decreased. These activities were restored to a greater extent in animals treated with energy-modulating vitamins. From these experimental results, one may hypothesize that the combination therapy of energy-modulating vitamins could be of major therapeutic value in breast cancer.

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Knauf, Felix, Nilufar Mohebbi, Carsten Teichert, Diana Herold, Blanka Rogina, Stephen Helfand, Maik Gollasch, Friedrich C. Luft, and Peter S. Aronson. "The life-extending gene Indy encodes an exchanger for Krebs-cycle intermediates." Biochemical Journal 397, no. 1 (June 14, 2006): 25–29. http://dx.doi.org/10.1042/bj20060409.

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A longevity gene called Indy (for ‘I'm not dead yet’), with similarity to mammalian genes encoding sodium–dicarboxylate cotransporters, was identified in Drosophila melanogaster. Functional studies in Xenopus oocytes showed that INDY mediates the flux of dicarboxylates and citrate across the plasma membrane, but the specific transport mechanism mediated by INDY was not identified. To test whether INDY functions as an anion exchanger, we examined whether substrate efflux is stimulated by transportable substrates added to the external medium. Efflux of [14C]citrate from INDY-expressing oocytes was greatly accelerated by the addition of succinate to the external medium, indicating citrate–succinate exchange. The succinate-stimulated [14C]citrate efflux was sensitive to inhibition by DIDS (4,4′-di-isothiocyano-2,2′-disulphonic stilbene), as demonstrated previously for INDY-mediated succinate uptake. INDY-mediated efflux of [14C]citrate was also stimulated by external citrate and oxaloacetate, indicating citrate–citrate and citrate–oxaloacetate exchange. Similarly, efflux of [14C]succinate from INDY-expressing oocytes was stimulated by external citrate, α-oxoglutarate and fumarate, indicating succinate–citrate, succinate–α-oxoglutarate and succinate–fumarate exchange respectively. Conversely, when INDY-expressing Xenopus oocytes were loaded with succinate and citrate, [14C]succinate uptake was markedly stimulated, confirming succinate–succinate and succinate–citrate exchange. Exchange of internal anion for external citrate was markedly pHo-dependent, consistent with the concept that citrate is co-transported with a proton. Anion exchange was sodium-independent. We conclude that INDY functions as an exchanger of dicarboxylate and tricarboxylate Krebs-cycle intermediates. The effect of decreasing INDY activity, as in the long-lived Indy mutants, may be to alter energy metabolism in a manner that favours lifespan extension.

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Donèche, Bernard, Françoise Roux, and Pascal Ribéreau-Gayon. "Dégradation de l'acide malique par Botrytis cinerea." Canadian Journal of Botany 63, no. 10 (October 1, 1985): 1820–24. http://dx.doi.org/10.1139/b85-257.

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During the growth of Botrytis cinerea on grape must, malic acid is actively oxidized by malic dehydrogenase. Some properties of this constitutive enzyme are described. In the absence of glucose, malic acid metabolism results in an equivalent accumulation of oxalic acid. In the presence of glucose, malic acid degradation is much slower, but the glucose is completely oxidized by the reactions of the Krebs cycle. Citric acid production in Czapek solution and in grape must differs according to strains of Botrytis cinerea; it depends mainly on glucose metabolism and is not directly related to malic acid degradation.

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Schumann, W. C., I. Magnusson, V. Chandramouli, K. Kumaran, J. Wahren, and B. R. Landau. "Metabolism of [2-14C]acetate and its use in assessing hepatic Krebs cycle activity and gluconeogenesis." Journal of Biological Chemistry 266, no. 11 (April 1991): 6985–90. http://dx.doi.org/10.1016/s0021-9258(20)89599-4.

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Sykes, Steven E., and Stephen L. Hajduk. "Dual Functions of α-Ketoglutarate Dehydrogenase E2 in the Krebs Cycle and Mitochondrial DNA Inheritance in Trypanosoma brucei." Eukaryotic Cell 12, no. 1 (November 2, 2012): 78–90. http://dx.doi.org/10.1128/ec.00269-12.

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ABSTRACT The dihydrolipoyl succinyltransferase (E2) of the multisubunit α-ketoglutarate dehydrogenase complex (α-KD) is an essential Krebs cycle enzyme commonly found in the matrices of mitochondria. African trypanosomes developmentally regulate mitochondrial carbohydrate metabolism and lack a functional Krebs cycle in the bloodstream of mammals. We found that despite the absence of a functional α-KD, bloodstream form (BF) trypanosomes express α-KDE2, which localized to the mitochondrial matrix and inner membrane. Furthermore, α-KDE2 fractionated with the mitochondrial genome, the kinetoplast DNA (kDNA), in a complex with the flagellum. A role for α-KDE2 in kDNA maintenance was revealed in α-KDE2 RNA interference (RNAi) knockdowns. Following RNAi induction, bloodstream trypanosomes showed pronounced growth reduction and often failed to equally distribute kDNA to daughter cells, resulting in accumulation of cells devoid of kDNA (dyskinetoplastic) or containing two kinetoplasts. Dyskinetoplastic trypanosomes lacked mitochondrial membrane potential and contained mitochondria of substantially reduced volume. These results indicate that α-KDE2 is bifunctional, both as a metabolic enzyme and as a mitochondrial inheritance factor necessary for the distribution of kDNA networks to daughter cells at cytokinesis.

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Hernández-Fisac, Inés, Sergio Fernández-Pascual, Henrik Ortsäter, Javier Pizarro-Delgado, Rafael Martín Del Río, Peter Bergsten, and Jorge Tamarit-Rodriguez. "Oxo-4-methylpentanoic acid directs the metabolism of GABA into the Krebs cycle in rat pancreatic islets." Biochemical Journal 400, no. 1 (October 27, 2006): 81–89. http://dx.doi.org/10.1042/bj20060173.

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OMP (oxo-4-methylpentanoic acid) stimulates by itself a biphasic secretion of insulin whereas L-leucine requires the presence of L-glutamine. L-Glutamine is predominantly converted into GABA (γ-aminobutyric acid) in rat islets and L-leucine seems to promote its metabolism in the ‘GABA shunt’ [Fernández-Pascual, Mukala-Nsengu-Tshibangu, Martín del Río and Tamarit-Rodríguez (2004) Biochem. J. 379, 721–729]. In the present study, we have investigated how 10 mM OMP affects L-glutamine metabolism to uncover possible differences with L-leucine that might help to elucidate whether they share a common mechanism of stimulation of insulin secretion. In contrast with L-leucine, OMP alone stimulated a biphasic insulin secretion in rat perifused islets and decreased the islet content of GABA without modifying its extracellular release irrespective of the concentration of L-glutamine in the medium. GABA was transaminated to L-leucine whose intracellular concentration did not change because it was efficiently transported out of the islet cells. The L-[U-14C]-Glutamine (at 0.5 and 10.0 mM) conversion to 14CO2 was enhanced by 10 mM OMP within 30% and 70% respectively. Gabaculine (250 μM), a GABA transaminase inhibitor, suppressed OMP-induced oxygen consumption but not L-leucine- or glucose-stimulated respiration. It also suppressed the OMP-induced decrease in islet GABA content and the OMP-induced increase in insulin release. These results support the view that OMP promotes islet metabolism in the ‘GABA shunt’ generating 2-oxo-glutarate, in the branched-chain α-amino acid transaminase reaction, which would in turn trigger GABA deamination by GABA transaminase. OMP, but not L-leucine, suppressed islet semialdehyde succinic acid reductase activity and this might shift the metabolic flux of the ‘GABA shunt’ from γ-hydroxybutyrate to succinic acid production.

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Telushkin, P. K., and P. P. Potapov. "Glycolysis intensity and activities of energy metabolism enzymes in the rat brain during repeated exposure to hypoglycemic doses of insulin." Problems of Endocrinology 40, no. 5 (December 15, 1994): 53–54. http://dx.doi.org/10.14341/probl12174.

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Renewable conditions of hypoglycemia are a frequent complication in the treatment of diabetes mellitus, determine the clinic of pancreatic insulinomas, are observed in diseases of the kidneys, liver, gastrointestinal tract and alcoholism, leading to the development of posthypoglycemic encephalopathy. At the same time, a single, even severe, insulin coma is accompanied by reversible metabolic changes in the brain. Therefore, the pathological features of metabolism in the nervous tissue, which are the result of repeated hypoglycemia, in particular possible disturbances in energy metabolism, require further study. In this work, we studied the main ways of glucose metabolism - the intensity of glycolysis and glycogenolysis, the activity of Krebs cycle dehydrogenases, alanine and aspartate aminotransferases in the rat brain in setting of multiple hypoglycemia.

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Keller, Markus A., Paul C. Driscoll, Christoph B. Messner, and Markus Ralser. "1H-NMR as implemented in several origin of life studies artificially implies the absence of metabolism-like non-enzymatic reactions by being signal-suppressed." Wellcome Open Research 2 (May 14, 2018): 52. http://dx.doi.org/10.12688/wellcomeopenres.12103.2.

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Background. Life depends on small subsets of chemically possible reactions. A chemical process can hence be prebiotically plausible, yet be unrelated to the origins of life. An example is the synthesis of nucleotides from hydrogen cyanide, considered prebiotically plausible, but incompatible with metabolic evolution. In contrast, only few metabolism-compatible prebiotic reactions were known until recently. Here, we question whether technical limitations may have contributed to the situation. Methods: Enzymes evolved to accelerate and control biochemical reactions. This situation dictates that compared to modern metabolic pathways, precursors to enzymatic reactions have been slower and less efficient, yielding lower metabolite quantities. This situation demands for the application of highly sensitive analytical techniques for studying ‘proto-metabolism’. We noticed that a set of proto-metabolism studies derive conclusions from the absence of metabolism-like signals, yet do not report detection limits. We here benchmark the respective 1H-NMR implementation for the ability to detect Krebs cycle intermediates, considered examples of plausible metabolic precursors. Results: Compared to metabolomics ‘gold-standard’ methods, 1H-NMR as implemented is i) at least one hundred- to thousand-fold less sensitive, ii) prone to selective metabolite loss, and iii) subject to signal suppression by Fe(II) concentrations as extrapolated from Archean sediment. In sum these restrictions mount to huge sensitivity deficits, so that even highly concentrated Krebs cycle intermediates are rendered undetectable unless the method is altered to boost sensitivity. Conclusions 1H-NMR as implemented in several origin of life studies does not achieve the sensitivity to detect cellular metabolite concentrations, let alone evolutionary precursors at even lower concentration. These studies can hence not serve as proof-of-absence for metabolism-like reactions. Origin of life theories that essentially depend on this assumption, i.e. those that consider proto-metabolism to consist of non-metabolism-like reactions derived from non-metabolic precursors like hydrogen cyanide, may have been derived from a misinterpretation of negative analytical results.

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Zhong, Min, Yinghui Yuan, Sheng Shu, Jin Sun, Shirong Guo, Ruonan Yuan, and Yuanyuan Tang. "Effects of exogenous putrescine on glycolysis and Krebs cycle metabolism in cucumber leaves subjected to salt stress." Plant Growth Regulation 79, no. 3 (November 12, 2015): 319–30. http://dx.doi.org/10.1007/s10725-015-0136-9.

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Phoboo, Susanna, Dipayan Sarkar, Prasanta C. Bhowmik, Pramod Kumar Jha, and Kalidas Shetty. "Improving salinity resilience in Swertia chirayita clonal line with Lactobacillus plantarum." Canadian Journal of Plant Science 96, no. 1 (February 1, 2016): 117–27. http://dx.doi.org/10.1139/cjps-2015-0178.

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Abstract:

Plants defense responses to abiotic stresses, including salinity stress, involve stimulation of defense related pathways such as biosynthesis of secondary metabolites and induction of endogenous antioxidant enzyme responses. In the present study, a single seed origin clonal line of Swertia chirayita inoculated with Lactobacillus plantarum (LP) was grown under different salinity levels. Control had no LP inoculation. S. chirayita inoculated with LP showed higher accumulation of proline, low proline dehydrogenase activity, up-regulation of pentose phosphate pathway, down-regulation of succinate dehydrogenase activity (Krebs cycle) and low total phenolic content with increased salt concentrations. In comparison, S. chirayita without LP adopted a different biochemical mechanism to counter salt stress (NaCl) by up-regulating both pentose phosphate pathway and Krebs cycle along with stimulation of phenolic biosynthesis. Guaiacol peroxidase (GPX) activity increased with and without LP treatment in response to increasing concentrations of salt. These results indicate that S. chirayita inoculated with LP exhibits a greater salinity stress tolerance than S. chirayita without LP by adopting a more energy efficient defense responses and potentially efficiently partitioning carbon flux between primary and secondary metabolism to counter salt induced oxidative stress.

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Dolan, Stephen K., and Martin Welch. "The Glyoxylate Shunt, 60 Years On." Annual Review of Microbiology 72, no. 1 (September 8, 2018): 309–30. http://dx.doi.org/10.1146/annurev-micro-090817-062257.

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Abstract:

2017 marks the 60th anniversary of Krebs’ seminal paper on the glyoxylate shunt (and coincidentally, also the 80th anniversary of his discovery of the citric acid cycle). Sixty years on, we have witnessed substantial developments in our understanding of how flux is partitioned between the glyoxylate shunt and the oxidative decarboxylation steps of the citric acid cycle. The last decade has shown us that the beautifully elegant textbook mechanism that regulates carbon flux through the shunt in E. coli is an oversimplification of the situation in many other bacteria. The aim of this review is to assess how this new knowledge is impacting our understanding of flux control at the TCA cycle/glyoxylate shunt branch point in a wider range of genera, and to summarize recent findings implicating a role for the glyoxylate shunt in cellular functions other than metabolism.

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Journal articles on the topic 'Krebs cycle metabolism'

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