Artykuły w czasopismach: „Citrate metabolism”

1

Monchi, Mehran. "Citrate pathophysiology and metabolism". Transfusion and Apheresis Science 56, nr 1 (luty 2017): 28–30. http://dx.doi.org/10.1016/j.transci.2016.12.013.

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Korithoski, Bryan, Kirsten Krastel i Dennis G. Cvitkovitch. "Transport and Metabolism of Citrate by Streptococcus mutans". Journal of Bacteriology 187, nr 13 (1.07.2005): 4451–56. http://dx.doi.org/10.1128/jb.187.13.4451-4456.2005.

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ABSTRACT Streptococcus mutans, a normal inhabitant of dental plaque, is considered a primary etiological agent of dental caries. Two virulence determinants of S. mutans are its acidogenicity and aciduricity (the ability to produce acid and the ability to survive and grow at low pH, respectively). Citric acid is ubiquitous in nature; it is a component of fruit juices, bones, and teeth. In lactic acid bacteria citrate transport has been linked to increased survival in acidic conditions. We identified putative citrate transport and metabolism genes in S. mutans, which led us to investigate citrate transport and metabolism. Our goals in this study were to determine the mechanisms of citrate transport and metabolism in S. mutans and to examine whether citrate modulates S. mutans aciduricity. Radiolabeled citrate was used during citrate transport to identify citrate metal ion cofactors, and thin-layer chromatography was used to identify metabolic end products of citrate metabolism. S. mutans was grown in medium MM4 with different citrate concentrations and pH values, and the effects on the growth rate and cell survival were monitored. Intracellular citrate inhibited the growth of the bacteria, especially at low pH. The most effective cofactor for citrate uptake by S. mutans was Fe3+. The metabolic end product of citrate metabolism was aspartate, and a citrate transporter mutant was more citrate tolerant than the parent.

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Chen, Fangfang, Hanna Friederike Willenbockel i Thekla Cordes. "Mapping the Metabolic Niche of Citrate Metabolism and SLC13A5". Metabolites 13, nr 3 (23.02.2023): 331. http://dx.doi.org/10.3390/metabo13030331.

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The small molecule citrate is a key molecule that is synthesized de novo and involved in diverse biochemical pathways influencing cell metabolism and function. Citrate is highly abundant in the circulation, and cells take up extracellular citrate via the sodium-dependent plasma membrane transporter NaCT encoded by the SLC13A5 gene. Citrate is critical to maintaining metabolic homeostasis and impaired NaCT activity is implicated in metabolic disorders. Though citrate is one of the best known and most studied metabolites in humans, little is known about the consequences of altered citrate uptake and metabolism. Here, we review recent findings on SLC13A5, NaCT, and citrate metabolism and discuss the effects on metabolic homeostasis and SLC13A5-dependent phenotypes. We discuss the “multiple-hit theory” and how stress factors induce metabolic reprogramming that may synergize with impaired NaCT activity to alter cell fate and function. Furthermore, we underline how citrate metabolism and compartmentalization can be quantified by combining mass spectrometry and tracing approaches. We also discuss species-specific differences and potential therapeutic implications of SLC13A5 and NaCT. Understanding the synergistic impact of multiple stress factors on citrate metabolism may help to decipher the disease mechanisms associated with SLC13A5 citrate transport disorders.

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Mortera, Pablo, Agata Pudlik, Christian Magni, Sergio Alarcón i Juke S. Lolkema. "Ca2+-Citrate Uptake and Metabolism in Lactobacillus casei ATCC 334". Applied and Environmental Microbiology 79, nr 15 (24.05.2013): 4603–12. http://dx.doi.org/10.1128/aem.00925-13.

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ABSTRACTThe putative citrate metabolic pathway inLactobacillus caseiATCC 334 consists of the transporter CitH, a proton symporter of the citrate-divalent metal ion family of transporters CitMHS, citrate lyase, and the membrane-bound oxaloacetate decarboxylase complex OAD-ABDH. Resting cells ofLactobacillus caseiATCC 334 metabolized citrate in complex with Ca2+and not as free citrate or the Mg2+-citrate complex, thereby identifying Ca2+-citrate as the substrate of the transporter CitH. The pathway was induced in the presence of Ca2+and citrate during growth and repressed by the presence of glucose and of galactose, most likely by a carbon catabolite repression mechanism. The end products of Ca2+-citrate metabolism by resting cells ofLb. caseiwere pyruvate, acetate, and acetoin, demonstrating the activity of the membrane-bound oxaloacetate decarboxylase complex OAD-ABDH. Following pyruvate, the pathway splits into two branches. One branch is the classical citrate fermentation pathway producing acetoin by α-acetolactate synthase and α-acetolactate decarboxylase. The other branch yields acetate, for which the route is still obscure. Ca2+-citrate metabolism in a modified MRS medium lacking a carbohydrate did not significantly affect the growth characteristics, and generation of metabolic energy in the form of proton motive force (PMF) was not observed in resting cells. In contrast, carbohydrate/Ca2+-citrate cometabolism resulted in a higher biomass yield in batch culture. However, also with these cells, no generation of PMF was associated with Ca2+-citrate metabolism. It is concluded that citrate metabolism inLb. caseiis beneficial when it counteracts acidification by carbohydrate metabolism in later growth stages.

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Cartledge, S., D. J. Candy i R. J. Hawker. "Citrate metabolism by human platelets". Transfusion Medicine 7, nr 3 (wrzesień 1997): 211–15. http://dx.doi.org/10.1046/j.1365-3148.1997.d01-28.x.

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Kanbe, Chiyuki, i Kinji Uchida. "Citrate Metabolism by Pediococcus halophilus". Applied and Environmental Microbiology 53, nr 6 (1987): 1257–62. http://dx.doi.org/10.1128/aem.53.6.1257-1262.1987.

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Antranikian, Garabed, i Friedrich Giffhorn. "Citrate metabolism in anaerobic bacteria". FEMS Microbiology Letters 46, nr 2 (czerwiec 1987): 175–98. http://dx.doi.org/10.1111/j.1574-6968.1987.tb02458.x.

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Sarantinopoulos, Panagiotis, George Kalantzopoulos i Effie Tsakalidou. "Citrate Metabolism by Enterococcus faecalis FAIR-E 229". Applied and Environmental Microbiology 67, nr 12 (1.12.2001): 5482–87. http://dx.doi.org/10.1128/aem.67.12.5482-5487.2001.

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ABSTRACT Citrate metabolism by Enterococcus faecalis FAIR-E 229 was studied in various growth media containing citrate either in the presence of glucose or lactose or as the sole carbon source. In skim milk (130 mM lactose, 8 mM citrate), cometabolism of citrate and lactose was observed from the first stages of the growth phase. Lactose was stoichiometrically converted into lactate, while citrate was converted into acetate, formate, and ethanol. When de Man-Rogosa-Sharpe (MRS) broth containing lactose (28 mM) instead of glucose was used,E. faecalis FAIR-E 229 catabolized only the carbohydrate. Lactate was the major end product, and small amounts of ethanol were also detected. Increasing concentrations of citrate (10, 40, 70, and 100 mM) added to MRS broth enhanced both the maximum growth rate ofE. faecalis FAIR-E 229 and glucose catabolism, although citrate itself was not catabolized. Glucose was converted stoichiometrically into lactate, while small amounts of ethanol were produced as well. Finally, when increasing initial concentrations of citrate (10, 40, 70, and 100 mM) were used as the sole carbon sources in MRS broth without glucose, the main end products were acetate and formate. Small amounts of lactate, ethanol, and acetoin were also detected. This work strongly supports the suggestion that enterococcal strains have the metabolic potential to metabolize citrate and therefore to actively contribute to the flavor development of fermented dairy products.

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9

Leandro, João G. B., Jair M. Espindola-Netto, Maria Carolina F. Vianna, Lilian S. Gomez, Thaina M. DeMaria, Monica M. Marinho-Carvalho, Patricia Zancan, Heitor A. Paula Neto i Mauro Sola-Penna. "Exogenous citrate impairs glucose tolerance and promotes visceral adipose tissue inflammation in mice". British Journal of Nutrition 115, nr 6 (11.02.2016): 967–73. http://dx.doi.org/10.1017/s0007114516000027.

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AbstractOverweight and obesity have become epidemic worldwide and are linked to sedentary lifestyle and the consumption of processed foods and drinks. Citrate is a metabolite that plays central roles in carbohydrate and lipid metabolism. In addition, citrate is the additive most commonly used by the food industry, and therefore is highly consumed. Extracellular citrate can freely enter the cells via the constitutively expressed plasma membrane citrate transporter. Within the cytosol, citrate is readily metabolised by ATP-citrate lyase into acetyl-CoA – the metabolic precursor of endogenously produced lipids and cholesterol. We therefore hypothesised that the citrate ingested from processed foods and drinks could contribute to increased postprandial fat production and weight gain. To test our hypothesis, we administered citrate to mice through their drinking water with or without sucrose and monitored their weight gain and other metabolic parameters. Our results showed that mice receiving citrate or citrate+sucrose did not show increased weight gain or an increase in the weight of the liver, skeletal muscles or adipose tissues (AT). Moreover, the plasma lipid profiles (TAG, total cholesterol, LDL and HDL) were similar across all groups. However, the group receiving citrate+sucrose showed augmented fasting glycaemia, glucose intolerance and the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6 and IL-10) in their AT. Therefore, our results suggest that citrate consumption contributes to increased AT inflammation and altered glucose metabolism, which is indicative of initial insulin resistance. Thus, citrate consumption could be a previously unknown causative agent for the complications associated with obesity.

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Pudlik, Agata M., i Juke S. Lolkema. "Rerouting Citrate Metabolism in Lactococcus lactis to Citrate-Driven Transamination". Applied and Environmental Microbiology 78, nr 18 (13.07.2012): 6665–73. http://dx.doi.org/10.1128/aem.01811-12.

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ABSTRACTOxaloacetate is an intermediate of the citrate fermentation pathway that accumulates in the cytoplasm ofLactococcus lactisILCitM(pFL3) at a high concentration due to the inactivation of oxaloacetate decarboxylase. An excess of toxic oxaloacetate is excreted into the medium in exchange for citrate by the citrate transporter CitP (A. M. Pudlik and J. S. Lolkema, J. Bacteriol. 193:4049–4056, 2011). In this study, transamination of amino acids with oxaloacetate as the keto donor is described as an additional mechanism to relieve toxic stress. Redirection of the citrate metabolic pathway into the transamination route in the presence of the branched-chain amino acids Ile, Leu, and Val; the aromatic amino acids Phe, Trp, and Tyr; and Met resulted in the formation of aspartate and the corresponding α-keto acids. Cells grown in the presence of citrate showed 3.5 to 7 times higher transaminase activity in the cytoplasm than cells grown in the absence of citrate. The study demonstrates that transaminases ofL. lactisaccept oxaloacetate as a keto donor. A significant fraction of 2-keto-4-methylthiobutyrate formed from methionine by citrate-driven transaminationin vivowas further metabolized, yielding the cheese aroma compounds 2-hydroxy-4-methylthiobutyrate and methyl-3-methylthiopropionate. Reducing equivalents required for the former compound were produced in the citrate fermentation pathway as NADH. Similarly, phenylpyruvate, the transamination product of phenylalanine, was reduced to phenyllactate, while the dehydrogenase activity was not observed for the branched-chain keto acids. Both α-keto acids and α-hydroxy acids are known substrates of CitP and may be excreted from the cell in exchange for citrate or oxaloacetate.

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NAKAMURA, Yumiko, Yasuhide TONOGAI, Sumiko TSUJI i Yoshio ITO. "Metabolism of Citric Acid, Potassium Citrate, Sodium Citrate and Calcium Citrate in the Rat". Food Hygiene and Safety Science (Shokuhin Eiseigaku Zasshi) 28, nr 4 (1987): 251–60. http://dx.doi.org/10.3358/shokueishi.28.251.

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Magni, Christian, Diego de Mendoza, Wil N. Konings i Juke S. Lolkema. "Mechanism of Citrate Metabolism inLactococcus lactis: Resistance against Lactate Toxicity at Low pH". Journal of Bacteriology 181, nr 5 (1.03.1999): 1451–57. http://dx.doi.org/10.1128/jb.181.5.1451-1457.1999.

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ABSTRACT Measurement of the flux through the citrate fermentation pathway in resting cells of Lactococcus lactis CRL264 grown in a pH-controlled fermentor at different pH values showed that the pathway was constitutively expressed, but its activity was significantly enhanced at low pH. The flux through the citrate-degrading pathway correlated with the magnitude of the membrane potential and pH gradient that were generated when citrate was added to the cells. The citrate degradation rate and proton motive force were significantly higher when glucose was metabolized at the same time, a phenomenon that could be mimicked by the addition of lactate, the end product of glucose metabolism. The results clearly demonstrate that citrate metabolism inL. lactis is a secondary proton motive force-generating pathway. Although the proton motive force generated by citrate in cells grown at low pH was of the same magnitude as that generated by glucose fermentation, citrate metabolism did not affect the growth rate of L. lactis in rich media. However, inhibition of growth by lactate was relieved when citrate also was present in the growth medium. Citrate did not relieve the inhibition by other weak acids, suggesting a specific role of the citrate transporter CitP in the relief of inhibition. The mechanism of citrate metabolism presented here provides an explanation for the resistance to lactate toxicity. It is suggested that the citrate metabolic pathway is induced under the acidic conditions of the late exponential growth phase to make the cells (more) resistant to the inhibitory effects of the fermentation product, lactate, that accumulates under these conditions.

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Vaningelgem, Frederik, Veerle Ghijsels, Effie Tsakalidou i Luc De Vuyst. "Cometabolism of Citrate and Glucose by Enterococcus faecium FAIR-E 198 in the Absence of Cellular Growth". Applied and Environmental Microbiology 72, nr 1 (styczeń 2006): 319–26. http://dx.doi.org/10.1128/aem.72.1.319-326.2006.

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ABSTRACT Citrate metabolism by Enterococcus faecium FAIR-E 198, an isolate from Greek Feta cheese, was studied in modified MRS (mMRS) medium under different pH conditions and glucose and citrate concentrations. In the absence of glucose, this strain was able to metabolize citrate in a pH range from constant pH 5.0 to 7.0. At a constant pH 8.0, no citrate was metabolized, although growth took place. The main end products of citrate metabolism were acetate, formate, acetoin, and carbon dioxide, whereas ethanol and diacetyl were present in smaller amounts. In the presence of glucose, citrate was cometabolized, but it did not contribute to growth. Also, more acetate and less acetoin were formed compared to growth in mMRS medium and in the absence of glucose. Most of the citrate was consumed during the stationary phase, indicating that energy generated by citrate metabolism was used for maintenance. Experiments with cell-free fermented mMRS medium indicated that E. faecium FAIR-E 198 was able to metabolize another energy source present in the medium.

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Li, Heng, Nancy E. Ramia, Frédéric Borges, Anne-Marie Revol-Junelles, Finn Kvist Vogensen i Jørgen J. Leisner. "Identification of Potential Citrate Metabolism Pathways in Carnobacterium maltaromaticum". Microorganisms 9, nr 10 (18.10.2021): 2169. http://dx.doi.org/10.3390/microorganisms9102169.

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In the present study, we describe the identification of potential citrate metabolism pathways for the lactic acid bacterium (LAB) Carnobacterium maltaromaticum. A phenotypic assay indicated that four of six C. maltaromaticum strains showed weak (Cm 6-1 and ATCC 35586) or even delayed (Cm 3-1 and Cm 5-1) citrate utilization activity. The remaining two strains, Cm 4-1 and Cm 1-2 gave negative results. Additional analysis showed no or very limited utilization of citrate in media containing 1% glucose and 22 or 30 mM citrate and inoculated with Cm 6-1 or ATCC 35586. Two potential pathways of citrate metabolism were identified by bioinformatics analyses in C. maltaromaticum including either oxaloacetate (pathway 1) or tricarboxylic compounds such as isocitrate and α-ketoglutarate (pathway 2) as intermediates. Genes encoding pathway 1 were present in two out of six strains while pathway 2 included genes present in all six strains. The two potential citrate metabolism pathways in C. maltaromaticum may potentially affect the sensory profiles of milk and soft cheeses subjected to growth with this species.

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Melnick, Joel Z., Patricia A. Preisig, Robert J. Alpern i Michel Baum. "Renal citrate metabolism and urinary citrate excretion in the infant rat". Kidney International 57, nr 3 (marzec 2000): 891–97. http://dx.doi.org/10.1046/j.1523-1755.2000.057003891.x.

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Yasukawa, Shu, Masato Takamatsu, Shoichi Ebisuno, Shigeyoshi Morimoto, Toshihiko Yoshida i Tadashi Ohkawa. "STUDIES ON CITRATE METABOLISM IN UROLITHIASIS". Japanese Journal of Urology 76, nr 12 (1985): 1848–54. http://dx.doi.org/10.5980/jpnjurol1928.76.12_1848.

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Yasukawa, Shu, Masaki Uehara, Shigeyoshi Morimoto, Toshihiko Yoshida, Toshiro Fukatani, Shoichi Ebisuno i Tadashi Ohkawa. "STUDIES OF CITRATE METABOLISM IN UROLITHIASIS". Japanese Journal of Urology 78, nr 4 (1987): 626–33. http://dx.doi.org/10.5980/jpnjurol1928.78.4_626.

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Icard, Philippe, Ludovic Fournel, Marco Alifano i Hubert Lincet. "Extracellular Citrate and Cancer Metabolism—Letter". Cancer Research 78, nr 17 (16.08.2018): 5176. http://dx.doi.org/10.1158/0008-5472.can-18-1666.

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Mycielska, Maria E., i Edward K. Geissler. "Extracellular Citrate and Cancer Metabolism—Response". Cancer Research 78, nr 17 (16.08.2018): 5177. http://dx.doi.org/10.1158/0008-5472.can-18-1899.

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Popova, Tatyana N., i Miguel Â. A. Pinheiro de Carvalho. "Citrate and isocitrate in plant metabolism". Biochimica et Biophysica Acta (BBA) - Bioenergetics 1364, nr 3 (maj 1998): 307–25. http://dx.doi.org/10.1016/s0005-2728(98)00008-5.

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Hugenholtz, Jeroen. "Citrate metabolism in lactic acid bacteria". FEMS Microbiology Reviews 12, nr 1-3 (wrzesień 1993): 165–78. http://dx.doi.org/10.1111/j.1574-6976.1993.tb00017.x.

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Rea, Mary C., i Timothy M. Cogan. "Glucose prevents citrate metabolism by enterococci". International Journal of Food Microbiology 88, nr 2-3 (grudzień 2003): 201–6. http://dx.doi.org/10.1016/s0168-1605(03)00181-8.

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Jaramillo-Martinez, Valeria, Sathish Sivaprakasam, Vadivel Ganapathy i Ina L. Urbatsch. "Drosophila INDY and Mammalian INDY: Major Differences in Transport Mechanism and Structural Features despite Mostly Similar Biological Functions". Metabolites 11, nr 10 (29.09.2021): 669. http://dx.doi.org/10.3390/metabo11100669.

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INDY (I’m Not Dead Yet) is a plasma membrane transporter for citrate, first identified in Drosophila. Partial deficiency of INDY extends lifespan in this organism in a manner similar to that of caloric restriction. The mammalian counterpart (NaCT/SLC13A5) also transports citrate. In mice, it is the total, not partial, absence of the transporter that leads to a metabolic phenotype similar to that caloric restriction; however, there is evidence for subtle neurological dysfunction. Loss-of-function mutations in SLC13A5 (solute carrier gene family 13, member A5) occur in humans, causing a recessive disease, with severe clinical symptoms manifested by neonatal seizures and marked disruption in neurological development. Though both Drosophila INDY and mammalian INDY transport citrate, the translocation mechanism differs, the former being a dicarboxylate exchanger for the influx of citrate2− in exchange for other dicarboxylates, and the latter being a Na+-coupled uniporter for citrate2−. Their structures also differ as evident from only ~35% identity in amino acid sequence and from theoretically modeled 3D structures. The varied biological consequences of INDY deficiency across species, with the beneficial effects predominating in lower organisms and detrimental effects overwhelming in higher organisms, are probably reflective of species-specific differences in tissue expression and also in relative contribution of extracellular citrate to metabolic pathways in different tissues

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Drexler, Konstantin, Katharina M. Schmidt, Katrin Jordan, Marianne Federlin, Vladimir M. Milenkovic, Gerhard Liebisch, Anna Artati i in. "Cancer-associated cells release citrate to support tumour metastatic progression". Life Science Alliance 4, nr 6 (23.03.2021): e202000903. http://dx.doi.org/10.26508/lsa.202000903.

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Citrate is important for lipid synthesis and epigenetic regulation in addition to ATP production. We have previously reported that cancer cells import extracellular citrate via the pmCiC transporter to support their metabolism. Here, we show for the first time that citrate is supplied to cancer by cancer-associated stroma (CAS) and also that citrate synthesis and release is one of the latter’s major metabolic tasks. Citrate release from CAS is controlled by cancer cells through cross-cellular communication. The availability of citrate from CAS regulated the cytokine profile, metabolism and features of cellular invasion. Moreover, citrate released by CAS is involved in inducing cancer progression especially enhancing invasiveness and organ colonisation. In line with the in vitro observations, we show that depriving cancer cells of citrate using gluconate, a specific inhibitor of pmCiC, significantly reduced the growth and metastatic spread of human pancreatic cancer cells in vivo and muted stromal activation and angiogenesis. We conclude that citrate is supplied to tumour cells by CAS and citrate uptake plays a significant role in cancer metastatic progression.

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Hooks, Mark A., J. William Allwood, Joanna K. D. Harrison, Joachim Kopka, Alexander Erban, Royston Goodacre i Janneke Balk. "Selective induction and subcellular distribution of ACONITASE 3 reveal the importance of cytosolic citrate metabolism during lipid mobilization in Arabidopsis". Biochemical Journal 463, nr 2 (22.09.2014): 309–17. http://dx.doi.org/10.1042/bj20140430.

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The cytosolic location of AtACO3 and its importance in citrate metabolism support the operation of the classic glyoxylate cycle and not direct mitochondrial metabolism of citrate during lipid mobilization in seedlings of oilseed plants, such as Arabidopsis.

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Sánchez, Claudia, Ana Rute Neves, João Cavalheiro, Margarida Moreira dos Santos, Nieves García-Quintáns, Paloma López i Helena Santos. "Contribution of Citrate Metabolism to the Growth of Lactococcus lactis CRL264 at Low pH". Applied and Environmental Microbiology 74, nr 4 (21.12.2007): 1136–44. http://dx.doi.org/10.1128/aem.01061-07.

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ABSTRACT Lactococcus lactis subsp. lactis biovar diacetylactis CRL264 is a natural strain isolated from cheese (F. Sesma, D. Gardiol, A. P. de Ruiz Holgado, and D. de Mendoza, Appl. Environ. Microbiol. 56:2099-2103, 1990). The effect of citrate on the growth parameters at a very acidic pH value was studied with this strain and with derivatives whose citrate uptake capacity was genetically manipulated. The culture pH was maintained at 4.5 to prevent alkalinization of the medium, a well-known effect of citrate metabolism. In the presence of citrate, the maximum specific growth rate and the specific glucose consumption rate were stimulated. Moreover, a more efficient energy metabolism was revealed by analysis of the biomass yields relative to glucose consumption or ATP production. Thus, it was shown that the beneficial effect of citrate on growth under acid stress conditions is not primarily due to the concomitant alkalinization of the medium but stems from less expenditure of ATP, derived from glucose catabolism, to achieve pH homeostasis. After citrate depletion, a deleterious effect on the final biomass was apparent due to organic acid accumulation, particularly acetic acid. On the other hand, citrate metabolism endowed cells with extra ability to counteract lactic and acetic acid toxicity. In vivo 13C nuclear magnetic resonance provided strong evidence for the operation of a citrate/lactate exchanger. Interestingly, the greater capacity for citrate transport correlated positively with the final biomass and growth rates of the citrate-utilizing strains. We propose that increasing the citrate transport capacity of CRL264 could be a useful strategy to improve further the ability of this strain to cope with strongly acidic conditions.

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Martin, Mauricio G., Christian Magni, Diego de Mendoza i Paloma López. "CitI, a Transcription Factor Involved in Regulation of Citrate Metabolism in Lactic Acid Bacteria". Journal of Bacteriology 187, nr 15 (1.08.2005): 5146–55. http://dx.doi.org/10.1128/jb.187.15.5146-5155.2005.

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ABSTRACT A large variety of lactic acid bacteria (LAB) can utilize citrate under fermentative conditions. Although much information concerning the metabolic pathways leading to citrate utilization by LAB has been gathered, the mechanisms regulating these pathways are obscure. In Weissella paramesenteroides (formerly called Leuconostoc paramesenteroides), transcription of the citMDEFCGRP citrate operon and the upstream divergent gene citI is induced by the presence of citrate in the medium. Although genetic experiments have suggested that CitI is a transcriptional activator whose activity can be modulated in response to citrate availability, specific details of the interaction between CitI and DNA remained unknown. In this study, we show that CitI recognizes two A+T-rich operator sites located between citI and citM and that the DNA-binding affinity of CitI is increased by citrate. Subsequently, this citrate signal propagation leads to the activation of the cit operon through an enhanced recruitment of RNA polymerase to its promoters. Our results indicate that the control of CitI by the cellular pools of citrate provides a mechanism for sensing the availability of citrate and adjusting the expression of the cit operon accordingly. In addition, this is the first reported example of a transcription factor directly functioning as a citrate-activated switch allowing the cell to optimize the generation of metabolic energy.

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Strijbis, Karin, i Ben Distel. "Intracellular Acetyl Unit Transport in Fungal Carbon Metabolism". Eukaryotic Cell 9, nr 12 (1.10.2010): 1809–15. http://dx.doi.org/10.1128/ec.00172-10.

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ABSTRACT Acetyl coenzyme A (acetyl-CoA) is a central metabolite in carbon and energy metabolism. Because of its amphiphilic nature and bulkiness, acetyl-CoA cannot readily traverse biological membranes. In fungi, two systems for acetyl unit transport have been identified: a shuttle dependent on the carrier carnitine and a (peroxisomal) citrate synthase-dependent pathway. In the carnitine-dependent pathway, carnitine acetyltransferases exchange the CoA group of acetyl-CoA for carnitine, thereby forming acetyl-carnitine, which can be transported between subcellular compartments. Citrate synthase catalyzes the condensation of oxaloacetate and acetyl-CoA to form citrate that can be transported over the membrane. Since essential metabolic pathways such as fatty acid β-oxidation, the tricarboxylic acid (TCA) cycle, and the glyoxylate cycle are physically separated into different organelles, shuttling of acetyl units is essential for growth of fungal species on various carbon sources such as fatty acids, ethanol, acetate, or citrate. In this review we summarize the current knowledge on the different systems of acetyl transport that are operational during alternative carbon metabolism, with special focus on two fungal species: Saccharomyces cerevisiae and Candida albicans.

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Isken, F., T. Schulz, M. Möhlig, A. Pfeiffer i M. Ristow. "Chemical Inhibition of Citrate Metabolism Alters Glucose Metabolism in Mice". Hormone and Metabolic Research 38, nr 8 (sierpień 2006): 543–45. http://dx.doi.org/10.1055/s-2006-949528.

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Patil, Shivaputra A., June A. Mayor i Ronald S. Kaplan. "Citrate transporter inhibitors: possible new anticancer agents". Future Medicinal Chemistry 14, nr 9 (maj 2022): 665–79. http://dx.doi.org/10.4155/fmc-2021-0341.

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The culmination of 80+ years of cancer research implicates the aberrant metabolism in tumor cells as a root cause of pathogenesis. Citrate is an essential molecule in intermediary metabolism, and its amplified availability to critical pathways in cancer cells via citrate transporters confers a high rate of cancer cell growth and proliferation. Inhibiting the plasma membrane and mitochondrial citrate transporters – whether individually, in combination, or partnered with complementary metabolic targets – in order to combat cancer may prove to be a consequential chemotherapeutic strategy. This review aims to summarize the use of different classes of citrate transporter inhibitors for anticancer activity, either individually or as part of a cocktail.

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Kennes, C., H. C. Dubourguler, G. Albagnac i E. J. Nyns. "Citrate metabolism byLactobacillus plantarumisolated from orange juice". Journal of Applied Bacteriology 70, nr 5 (maj 1991): 380–84. http://dx.doi.org/10.1111/j.1365-2672.1991.tb02952.x.

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Igamberdiev, Abir U. "Citrate valve integrates mitochondria into photosynthetic metabolism". Mitochondrion 52 (maj 2020): 218–30. http://dx.doi.org/10.1016/j.mito.2020.04.003.

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Mycielska, Maria E., Ameet Patel, Nahit Rizaner, Maciej P. Mazurek, Hector Keun, Anup Patel, Vadivel Ganapathy i Mustafa B. A. Djamgoz. "Citrate transport and metabolism in mammalian cells". BioEssays 31, nr 1 (styczeń 2009): 10–20. http://dx.doi.org/10.1002/bies.080137.

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Vezzoli, Giuseppe, Giulia Magni, Monica Avino i Teresa Arcidiacono. "Ruolo del citrato nel metabolismo osseo". Giornale di Clinica Nefrologica e Dialisi 32, nr 1 (20.02.2020): 15–20. http://dx.doi.org/10.33393/gcnd.2020.991.

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Citrate is an organic compound involved in tricarboxylic acid cycle, regulation of acid-base balance, lipid metabolism and bone formation. The 90% of body citrate is deposited in bone tissue and is released with calcium ions during bone resorption; therefore, bone resorption contributes to maintain normal plasma levels of citrate together with kidney excretion. The parallel release of citrate and calcium from bones decreases the possibility of calcium-phosphate precipitation in soft tissues, as citrate can bind calcium ions in organic fluids. Citrate may also take part to the bone formation as it sustains the correct mineralization of bone organic matrix: its molecule binds calcium ions at the surface of hydroxyapatite nanocrystals and maintains the correct spatial disposition of nanocrystals, thus, stabilizing the structure of bone lamellae and sustaining biomechanical characteristics of bone tissue. Multiple studies observed that citrate administration significantly increased areal and volumetric bone mineral density at different locations of 1-2% per year and improved bone resorption markers as well. Therefore, it has been hypothesised a therapeutic role of citrate in osteoporosis; however, this role has to be better clarified to understand its real anti-fracture effect.

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Cabral, María E., María C. Abeijón Mukdsi, Roxana B. Medina de Figueroa i Silvia N. González. "Citrate metabolism by Enterococcus faecium and Enterococcus durans isolated from goat’s and ewe’s milk: influence of glucose and lactose". Canadian Journal of Microbiology 53, nr 5 (maj 2007): 607–15. http://dx.doi.org/10.1139/w07-011.

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Citrate metabolism by Enterococcus faecium ET C9 and Enterococcus durans Ov 421 was studied as sole energy source and in presence of glucose or lactose. Both strains utilized citrate as the sole energy source. Enterococcus faecium ET C9 showed diauxic growth in the presence of a limiting concentration of glucose. Neither strain used citrate until glucose was fully metabolized. The strains showed co-metabolism of citrate and lactose. Lactate, acetate, formate, and flavour compounds (diacetyl, acetoin, and 2,3-butanediol) were detected in both strains. The highest production of flavour compounds was detected during growth of E. durans Ov 421 in media supplemented with citrate–glucose and citrate–lactose. Citrate lyase was inducible in both strains. Acetate kinase activities presented the highest values in LAPTc medium, with E. faecium ET C9 displaying a specific activity 2.4-fold higher than E. durans. The highest levels of α-acetolactate synthase specific activity were detected in E. durans grown in LAPTc+g, in accordance with the maximum production of flavour compounds detected in this medium. Diacetyl and acetoinreductases displayed lower specific activity values in the presence of citrate. Enterococcus faecium and E. durans displayed citrate lyase, acetate kinase, α-acetolactate synthase, and diacetyl and acetoin reductase activities. These enzymes are necessary for conversion of citrate to flavour compounds that are important in fermented dairy products.

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Wiegand, Anna, Gioia Fischer, Harald Seeger, Daniel Fuster, Nasser Dhayat, Olivier Bonny, Thomas Ernandez, Min-Jeong Kim, Carsten A. Wagner i Nilufar Mohebbi. "Impact of potassium citrate on urinary risk profile, glucose and lipid metabolism of kidney stone formers in Switzerland". Clinical Kidney Journal 13, nr 6 (19.08.2019): 1037–48. http://dx.doi.org/10.1093/ckj/sfz098.

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Abstract Background Hypocitraturia and hypercalciuria are the most prevalent risk factors in kidney stone formers (KSFs). Citrate supplementation has been introduced for metaphylaxis in KSFs. However, beyond its effects on urinary parameters and stone recurrence, only a few studies have investigated the impact of citrate on other metabolic pathways such as glucose or lipid metabolism. Methods We performed an observational study using data from the Swiss Kidney Stone Cohort. Patients were subdivided into two groups based on treatment with potassium citrate or not. The outcomes were changes of urinary risk parameters, haemoglobin A1c (HbA1c), fasting glucose, cholesterol and body mass index (BMI). Results Hypocitraturia was present in 19.3% of 428 KSFs and potassium citrate was administered to 43 patients (10.0%) at a mean dosage of 3819 ± 1796 mg/day (corresponding to 12.5 ± 5.9 mmol/ day). Treatment with potassium citrate was associated with a significantly higher mean change in urinary citrate (P = 0.010) and urinary magnesium (P = 0.020) compared with no potassium citrate treatment. Exogenous citrate administration had no effect on cholesterol, fasting glucose, HbA1c and BMI. Multiple linear regression analysis demonstrated no significant association of 1,25-dihydroxyvitamin D3 [1,25(OH)2 D3] levels with urinary citrate excretion. Conclusion Potassium citrate supplementation in KSFs in Switzerland resulted in a beneficial change of the urinary risk profile by particularly increasing anti-lithogenic factors. Fasting glucose, HbA1c, cholesterol levels and BMI were unaffected by potassium citrate therapy after 3 months, suggesting that potassium citrate is safe and not associated with unfavourable metabolic side effects. Lastly, 1,25(OH)2 D3 levels were not associated with urinary citrate excretion.

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Bandell, M., M. E. Lhotte, C. Marty-Teysset, A. Veyrat, H. PrÃ¯Â¿Â½vost, V. Dartois, C. DiviÃ¯Â¿Â½s, W. N. Konings i J. S. Lolkema. "Mechanism of the Citrate Transporters in Carbohydrate and Citrate Cometabolism in Lactococcus andLeuconostoc Species". Applied and Environmental Microbiology 64, nr 5 (1.05.1998): 1594–600. http://dx.doi.org/10.1128/aem.64.5.1594-1600.1998.

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ABSTRACT Citrate metabolism in the lactic acid bacterium Leuconostoc mesenteroides generates an electrochemical proton gradient across the membrane by a secondary mechanism (C. Marty-Teysset, C. Posthuma, J. S. Lolkema, P. Schmitt, C. Divies, and W. N. Konings, J. Bacteriol. 178:2178–2185, 1996). Reports on the energetics of citrate metabolism in the related organism Lactococcus lactis are contradictory, and this study was performed to clarify this issue. Cloning of the membrane potential-generating citrate transporter (CitP) of Leuconostoc mesenteroides revealed an amino acid sequence that is almost identical to the known sequence of the CitP ofLactococcus lactis. The cloned gene was expressed in aLactococcus lactis Cit− strain, and the gene product was functionally characterized in membrane vesicles. Uptake of citrate was counteracted by the membrane potential, and the transporter efficiently catalyzed heterologous citrate-lactate exchange. These properties are essential for generation of a membrane potential under physiological conditions and show that the Leuconostoc CitP retains its properties when it is embedded in the cytoplasmic membrane of Lactococcus lactis. Furthermore, using the same criteria and experimental approach, we demonstrated that the endogenous CitP ofLactococcus lactis has the same properties, showing that the few differences in the amino acid sequences of the CitPs of members of the two genera do not result in different catalytic mechanisms. The results strongly suggest that the energetics of citrate degradation inLactococcus lactis and Leuconostoc mesenteroides are the same; i.e., citrate metabolism inLactococcus lactis is a proton motive force-generating process.

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Pashchenko, A. G., I. I. Kovalchuk i R. S. Fedoruk. "Mineral composition of the organism tissues and honeycombs of melliferous bees under the conditions of feeding them soybean flour and citrates of Cobalt and Nickel". Scientific Messenger of LNU of Veterinary Medicine and Biotechnology 21, nr 93 (2.04.2019): 60–64. http://dx.doi.org/10.32718/nvlvet9311.

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The inadequacy of mineral nutrition leads to inhibition of physiological and metabolic reactions in the body of honeybees. It is known that Cobalt chloride is used to activate oviposition of the queen bee. It was established that Cobalt and Nickel citrate, obtained by the method of nanotechnology, corrects the mineral metabolism and affects the metabolism of bees. It is known that Cobalt plays an important role in the work of enzymes; synthesis of vitamin B12, promotes assimilation of vitamins A, E, C; increases protein metabolism, participates in hematopoiesis. Nickel also has a pronounced effect on hemopoiesis, namely on the morphological composition of blood. But its effect on the cell and subcellular level is not well understood. The results of studies of the effect of soybean flour with the addition of Cobalt and Nickel citrates on the content of mineral elements in the tissues of the body of bees and honeycombs are given. The research was carried out in the farms in the Lviv region, in April-May at the bees of the Carpathian breed. It was established that the content of Ferrum, Cuprum and Germanium in the tissues of bees increases with the addition of soybean flour with Сobalt citrate at a dose of 2 mg per 500 g of soy flour. When Nickel citrate was added to the feed at a dose of 1 mg per 500 g of soy flour, the content of Ferrum and Cuprum increased in honeycombs. The complex combination of Citrits Co and Ni, soy flour with sugar syrup was characterized by a decrease in the level of Zn in the tissues of the bees compared to its contents in the control group samples. In samples of biological material, the content of Сobalt, Nickel and the essential elements Cuprum, Zink, Ferrum, Selenium, Germanium was determined by atomic emission spectrometry with inductively coupled plasma. Citrates of the microelements were produced by the method of M. Kosinov and V. Kaplunenkо.

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DEBORDE, CATHERINE, DOMINIQUE B. ROLIN, ARNAUD BONDON, JACQUES D. DE CERTAINES i PATRICK BOYAVAL. "In vivo nuclear magnetic resonance study of citrate metabolism in Propionibacterium freudenreichii subsp. shermanii". Journal of Dairy Research 65, nr 3 (sierpień 1998): 503–14. http://dx.doi.org/10.1017/s0022029998002878.

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Citrate metabolism by resting cells of Propionibacterium freudenreichii subsp. shermanii was investigated. In vivo13C nuclear magnetic resonance spectroscopy was used to study the pathway of citrate breakdown and to probe its utilization, non-invasively, in living cell suspensions. [2,4-13C]citrate was metabolized by resting cells to glutamate labelled in positions 2 and 4. In the presence of lactate or pyruvate, its rate of consumption was faster, but it was still converted to glutamate. No catabolic pathway other than the first third of a turn of the tricarboxylic acid cycle was used by Prop. freudenreichii subsp. shermanii to degrade citrate.

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Susilaningsih, Dwi, Asahedi Umoro, Fredrick Onyango Ochieng, Dian Noverita Widyaningrum, Hani Susanti, Hadi Susilo, I. Nengah Swastika i Utut Widyastuti. "ISOLASI GEN SITRAT SINTASE BAKTERI Pseudomonas aerugenosa PS2 DARI RIZOSFER POHON KRUING (Dipterocarpus sp.) UNTUK MODEL KONSTRUKSI METABOLISME SEL MIKROALGA BERKARBOHIDRAT RENDAH". BERITA BIOLOGI 18, nr 2 (27.08.2019): 247–53. http://dx.doi.org/10.14203/beritabiologi.v18i2.2967.

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Pseudomonas has the potential ability for production of citrate synthase synthesis. Pseudomonas aeruginosa could synthesize the enzyme of citrate synthase which is most likely compatible with microalgae cell. Pseudomonas aerugenosa can be found in the rhizosphere of Kruing (Dipterocarpus sp., Dipterocarpaceae). This bacteria is commonly used in agriculture purposes because it is able to synthesize organic acid such as citric acid. These organic acids are synthesized from a reaction between oxaloacetate and acetyl CoA, catalyzed by citrate synthase (CS) in the tricarboxylic acid cycle (TCA). Rhizosphere as microbial sources was obtained from Kruing (Dipterocarpus sp.), which was collected from ‘Carita’ Research Forest, Pandeglang, Banten, West Java. Citrate synthase gene-specific primers were designed based on citrate synthase gene sequences as depicted in Genbank. The isolation and amplification showed that citrate synthase can be detected and purified from Pseudomonas aeruginosa target and it consists of 1600 bp and encodes 509 amino acids. Based on BLAST (Basic Local Alignment Search Tool) analysis, CS genes that were successfully isolated had 92 % similarity with Pseudomonas aeruginosa type II citrate synthase. This CS gene is expected to be expressed in microalgae metabolism to divert the metabolism of carbohydrate formation into fatty acids.

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Huang, Qingyu, Jie Zhang, Lianzhong Luo, Xiaofei Wang, Xiaoxue Wang, Ambreen Alamdar, Siyuan Peng, Liangpo Liu, Meiping Tian i Heqing Shen. "Metabolomics reveals disturbed metabolic pathways in human lung epithelial cells exposed to airborne fine particulate matter". Toxicology Research 4, nr 4 (2015): 939–47. http://dx.doi.org/10.1039/c5tx00003c.

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Parkinson, E. Kenneth, Jerzy Adamski, Grit Zahn, Andreas Gaumann, Fabian Flores-Borja, Christine Ziegler i Maria E. Mycielska. "Extracellular citrate and metabolic adaptations of cancer cells". Cancer and Metastasis Reviews 40, nr 4 (grudzień 2021): 1073–91. http://dx.doi.org/10.1007/s10555-021-10007-1.

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Abstract It is well established that cancer cells acquire energy via the Warburg effect and oxidative phosphorylation. Citrate is considered to play a crucial role in cancer metabolism by virtue of its production in the reverse Krebs cycle from glutamine. Here, we review the evidence that extracellular citrate is one of the key metabolites of the metabolic pathways present in cancer cells. We review the different mechanisms by which pathways involved in keeping redox balance respond to the need of intracellular citrate synthesis under different extracellular metabolic conditions. In this context, we further discuss the hypothesis that extracellular citrate plays a role in switching between oxidative phosphorylation and the Warburg effect while citrate uptake enhances metastatic activities and therapy resistance. We also present the possibility that organs rich in citrate such as the liver, brain and bones might form a perfect niche for the secondary tumour growth and improve survival of colonising cancer cells. Consistently, metabolic support provided by cancer-associated and senescent cells is also discussed. Finally, we highlight evidence on the role of citrate on immune cells and its potential to modulate the biological functions of pro- and anti-tumour immune cells in the tumour microenvironment. Collectively, we review intriguing evidence supporting the potential role of extracellular citrate in the regulation of the overall cancer metabolism and metastatic activity.

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Icard, Philippe, Antoine Coquerel, Zherui Wu, Joseph Gligorov, David Fuks, Ludovic Fournel, Hubert Lincet i Luca Simula. "Understanding the Central Role of Citrate in the Metabolism of Cancer Cells and Tumors: An Update". International Journal of Molecular Sciences 22, nr 12 (19.06.2021): 6587. http://dx.doi.org/10.3390/ijms22126587.

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Citrate plays a central role in cancer cells’ metabolism and regulation. Derived from mitochondrial synthesis and/or carboxylation of α-ketoglutarate, it is cleaved by ATP-citrate lyase into acetyl-CoA and oxaloacetate. The rapid turnover of these molecules in proliferative cancer cells maintains a low-level of citrate, precluding its retro-inhibition on glycolytic enzymes. In cancer cells relying on glycolysis, this regulation helps sustain the Warburg effect. In those relying on an oxidative metabolism, fatty acid β-oxidation sustains a high production of citrate, which is still rapidly converted into acetyl-CoA and oxaloacetate, this latter molecule sustaining nucleotide synthesis and gluconeogenesis. Therefore, citrate levels are rarely high in cancer cells. Resistance of cancer cells to targeted therapies, such as tyrosine kinase inhibitors (TKIs), is frequently sustained by aerobic glycolysis and its key oncogenic drivers, such as Ras and its downstream effectors MAPK/ERK and PI3K/Akt. Remarkably, in preclinical cancer models, the administration of high doses of citrate showed various anti-cancer effects, such as the inhibition of glycolysis, the promotion of cytotoxic drugs sensibility and apoptosis, the neutralization of extracellular acidity, and the inhibition of tumors growth and of key signalling pathways (in particular, the IGF-1R/AKT pathway). Therefore, these preclinical results support the testing of the citrate strategy in clinical trials to counteract key oncogenic drivers sustaining cancer development and resistance to anti-cancer therapies.

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Li, Longlong, Mengling Peng, Chongyang Ge, Lei Yu i Haitian Ma. "(-)-Hydroxycitric Acid Reduced Lipid Droplets Accumulation Via Decreasing Acetyl-Coa Supply and Accelerating Energy Metabolism in Cultured Primary Chicken Hepatocytes". Cellular Physiology and Biochemistry 43, nr 2 (2017): 812–31. http://dx.doi.org/10.1159/000481564.

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Background/Aims: (-)-Hydroxycitric acid (HCA) had been shown to suppress fat accumulation in animals and humans, while the underlying biochemical mechanism is not fully understood, especially little information is available on whether (-)-HCA regulates energy metabolism and consequently affects fat deposition. Methods: Hepatocytes were cultured for 24 h and then exposed to (-)-HCA (0, 1, 10, 50 µM), enzyme protein content was determined by ELISA; lipid metabolism gene mRNA levels were detected by RT-PCR. Results: (-)-HCA significantly decreased the number and total area of lipid droplets. ATP-citrate lyase, fatty acid synthase and sterol regulatory element binding protein-1c mRNA level were significantly decreased after (-)-HCA treatment, whereas peroxisome proliferator-activated receptor α mRNA level was significantly increased. (-)-HCA significantly decreased ATP-citrate lyase activity and acetyl-CoA content in cytosol, but significantly increased glucose consumption and mitochondrial oxygen consumption rate. (-)-HCA promoted the activity/content of glucokinase, phosphofructokinase-1, pyruvate kinase, pyruvate dehydrogenase, citrate synthase, aconitase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase and ATP synthase remarkably. Conclusions: (-)-HCA decreased lipid droplets accumulation by reducing acetyl-CoA supply, which mainly achieved via inhibition of ATP-citrate lyase, and accelerating energy metabolism in chicken hepatocytes. These results proposed a biochemical mechanism of fat reduction by (-)-HCA in broiler chickens in term of energy metabolism.

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Bond, Daniel R., Tünde Mester, Camilla L. Nesbø, Andrea V. Izquierdo-Lopez, Frank L. Collart i Derek R. Lovley. "Characterization of Citrate Synthase from Geobacter sulfurreducens and Evidence for a Family of Citrate Synthases Similar to Those of Eukaryotes throughout the Geobacteraceae". Applied and Environmental Microbiology 71, nr 7 (lipiec 2005): 3858–65. http://dx.doi.org/10.1128/aem.71.7.3858-3865.2005.

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ABSTRACT Members of the family Geobacteraceae are commonly the predominant Fe(III)-reducing microorganisms in sedimentary environments, as well as on the surface of energy-harvesting electrodes, and are able to effectively couple the oxidation of acetate to the reduction of external electron acceptors. Citrate synthase activity of these organisms is of interest due to its key role in acetate metabolism. Prior sequencing of the genome of Geobacter sulfurreducens revealed a putative citrate synthase sequence related to the citrate synthases of eukaryotes. All citrate synthase activity in G. sulfurreducens could be resolved to a single 49-kDa protein via affinity chromatography. The enzyme was successfully expressed at high levels in Escherichia coli with similar properties as the native enzyme, and kinetic parameters were comparable to related citrate synthases (k cat = 8.3 s−1; Km = 14.1 and 4.3 μM for acetyl coenzyme A and oxaloacetate, respectively). The enzyme was dimeric and was slightly inhibited by ATP (Ki = 1.9 mM for acetyl coenzyme A), which is a known inhibitor for many eukaryotic, dimeric citrate synthases. NADH, an allosteric inhibitor of prokaryotic hexameric citrate synthases, did not affect enzyme activity. Unlike most prokaryotic dimeric citrate synthases, the enzyme did not have any methylcitrate synthase activity. A unique feature of the enzyme, in contrast to citrate synthases from both eukaryotes and prokaryotes, was a lack of stimulation by K+ ions. Similar citrate synthase sequences were detected in a diversity of other Geobacteraceae members. This first characterization of a eukaryotic-like citrate synthase from a prokaryote provides new insight into acetate metabolism in Geobacteraceae members and suggests a molecular target for tracking the presence and activity of these organisms in the environment.

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Iacobazzi, Vito, i Vittoria Infantino. "Citrate – new functions for an old metabolite". Biological Chemistry 395, nr 4 (1.04.2014): 387–99. http://dx.doi.org/10.1515/hsz-2013-0271.

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Abstract Citrate is an important substrate in cellular energy metabolism. It is produced in the mitochondria and used in the Krebs cycle or released into cytoplasm through a specific mitochondrial carrier, CIC. In the cytosol, citrate and its derivatives, acetyl-CoA and oxaloacetate, are used in normal and pathological processes. Beyond the classical role as metabolic regulator, recent studies have highlighted that citrate is involved in inflammation, cancer, insulin secretion, histone acetylation, neurological disorders, and non-alcoholic fatty liver disease. Monitoring changes in the citrate levels could therefore potentially be used as diagnostic tool. This review highlights these new aspects of citrate functions.

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Karp, Heini J., Maarit E. Ketola i Christel J. E. Lamberg-Allardt. "Acute effects of calcium carbonate, calcium citrate and potassium citrate on markers of calcium and bone metabolism in young women". British Journal of Nutrition 102, nr 9 (19.06.2009): 1341–47. http://dx.doi.org/10.1017/s0007114509990195.

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Both K and Ca supplementation may have beneficial effects on bone through separate mechanisms. K in the form of citrate or bicarbonate affects bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and bone metabolism in young women. Twelve healthy women aged 22–30 years were randomised into four controlled 24 h study sessions, each subject serving as her own control. At the beginning of each session, subjects received a single dose of calcium carbonate, calcium citrate, potassium citrate or a placebo in randomised order. The diet during each session was identical, containing 300 mg Ca. Both the calcium carbonate and calcium citrate supplement contained 1000 mg Ca; the potassium citrate supplement contained 2250 mg K. Markers of Ca and bone metabolism were followed. Potassium citrate decreased the bone resorption marker (N-terminal telopeptide of type I collagen) and increased Ca retention relative to the control session. Both Ca supplements decreased S-PTH concentration. Ca supplements also decreased bone resorption relative to the control session, but this was significant only for calcium carbonate. No differences in bone formation marker (bone-specific alkaline phosphatase) were seen among the study sessions. The results suggest that potassium citrate has a positive effect on the resorption marker despite low Ca intake. Both Ca supplements were absorbed well and decreased S-PTH efficiently.

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Miglionico, Rocchina, Ilenia Matera, Giovanna Maria Ventola, Giovanna Marchese, Vittorio Abruzzese, Magnus Monné, Angela Ostuni i Faustino Bisaccia. "Gene Expression Reprogramming by Citrate Supplementation Reduces HepG2 Cell Migration and Invasion". International Journal of Molecular Sciences 25, nr 12 (13.06.2024): 6509. http://dx.doi.org/10.3390/ijms25126509.

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Citrate, which is obtained from oxaloacetate and acetyl-CoA by citrate synthase in mitochondria, plays a key role in both normal and cancer cell metabolism. In this work, we investigated the effect of 10 mM extracellular citrate supplementation on HepG2 cells. Gene expression reprogramming was evaluated by whole transcriptome analysis using gene set enrichment analysis (GSEA). The transcriptomic data were validated through analyzing changes in the mRNA levels of selected genes by qRT-PCR. Citrate-treated cells exhibited the statistically significant dysregulation of 3551 genes; 851 genes were upregulated and 822 genes were downregulated. GSEA identified 40 pathways affected by differentially expressed mRNAs. The most affected biological processes were related to lipid and RNA metabolism. Several genes of the cytochrome P450 family were upregulated in treated cells compared to controls, including the CYP3A5 gene, a tumor suppressor in hepatocellular carcinoma (HCC) that plays an important protective role in HCC metastasis. The citrate-induced dysregulation of cytochromes could both improve the effectiveness of chemotherapeutics used in combination and reduce the aggressiveness of tumors by diminishing cell migration and invasion.

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Bott, Michael, Margareta Meyer i Peter Dimroth. "Regulation of anaerobic citrate metabolism in Klebsiella pneumoniae". Molecular Microbiology 18, nr 3 (listopad 1995): 533–46. http://dx.doi.org/10.1111/j.1365-2958.1995.mmi_18030533.x.

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Bott, M. "Anaerobic citrate metabolism and its regulation in enterobacteria". Archives of Microbiology 167, nr 2-3 (7.03.1997): 78–88. http://dx.doi.org/10.1007/s002030050419.

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