scholarly journals Metabolism of [3-13C]pyruvate and [3-13C]propionate in normal and ischaemic rat heart in vivo: 1H- and 13C-NMR studies

1995 ◽  
Vol 312 (1) ◽  
pp. 75-81 ◽  
Author(s):  
B Sumegi ◽  
B Podanyi ◽  
P Forgo ◽  
K E Kover
Keyword(s):  
Citric Acid ◽  
13C Nmr ◽  
Rat Heart ◽  
Citric Acid Cycle ◽  
Nmr Studies ◽  
Acetyl Coa ◽  
1H And 13C Nmr ◽  
Acid Cycle ◽  
Propionyl Carnitine

The oxidation of [3-13C]pyruvate and [3-13C]propionate was studied in vivo in infused rats. The infused [3-13C]pyruvate was quickly converted to [3-13C]lactate in the blood, and the [3-13C]lactate formed was well metabolized in both normoxic and ischaemic hearts. Large differences (200-600%) in the 13C enrichment of alanine (C-3) and acetyl-CoA (C-2) compared with lactate (C-3) were found in both normoxic and ischaemic hearts, suggesting that the extracellular [3-13C]lactate preferentially entered a region of the cytoplasm which specifically transfers the labelled pyruvate (formed from [3-13C]lactate) to the mitochondria. The highly enriched mitochondrial pyruvate gave high enrichment in alanine and acetyl-CoA, which was detected by 1H- and 13C-NMR spectroscopy. Ischaemia increased 13C incorporation into the main cytoplasmic lactate pool and decreased 13C incorporation into citric acid cycle intermediates, mainly decreasing the pyruvate anaplerosis. Isoprenaline-induced ischaemia of the heart caused only a slight decrease in pyruvate oxidation. In contrast to the decreased anaplerosis of pyruvate, the anaplerosis of propionate (and propionyl-carnitine) increased significantly in ischaemic hearts, which may contribute to the protective effect of propionyl-carnitine seen in ischaemia. In addition, we found that [3-13C]propionate preferentially labelled aspartate C-3 in rat heart, suggesting incomplete randomization of label in the succinyl-CoA-malate span of the citric acid cycle. These data show that proton observed 13C edited spectroscopic methods, i.e. heteronuclear spin-echo and the one-dimensional heteronuclear multiple quantum coherence sequence, can be successfully used to study heart metabolism in vivo.

13C-NMR spectroscopic evaluation of the citric acid cycle flux in conditions of high aspartate transaminase activity in glucose-perfused rat hearts

Biochimie ◽  
1998 ◽  
Vol 80 (12) ◽  
pp. 1013-1024 ◽  
Author(s):  
Son Tran-Dinh ◽  
Jacqueline A. Hoerter ◽  
Philippe Mateo ◽  
Franck Gyppaz ◽  
Martine Herve
Keyword(s):  
Citric Acid ◽  
13C Nmr ◽  
Citric Acid Cycle ◽  
Aspartate Transaminase ◽  
Transaminase Activity ◽  
Acid Cycle ◽  
Rat Hearts ◽  
Perfused Rat Hearts

scholarly journals Probing the Origin of Acetyl-CoA and Oxaloacetate Entering the Citric Acid Cycle from the13C Labeling of Citrate Released by Perfused Rat Hearts

1997 ◽  
Vol 272 (42) ◽  
pp. 26117-26124 ◽  
Author(s):  
Blandine Comte ◽  
Geneviève Vincent ◽  
Bertrand Bouchard ◽  
Christine Des Rosiers
Keyword(s):  
Citric Acid ◽  
Citric Acid Cycle ◽  
Acetyl Coa ◽  
Acid Cycle ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Carbon Isotope Fractionation by Autotrophic Bacteria with Three Different C02 Fixation Pathways

1989 ◽  
Vol 44 (5-6) ◽  
pp. 397-402 ◽  
Author(s):  
Andrea Preuß ◽  
Rolf Schauder ◽  
Georg Fuchs ◽  
Willibald Stichler
Keyword(s):  
Citric Acid ◽  
Carbon Isotope ◽  
Isotope Fractionation ◽  
Citric Acid Cycle ◽  
Pentose Phosphate ◽  
Acetobacterium Woodii ◽  
Acetyl Coa ◽  
Acid Cycle ◽  
Acetyl Coa Pathway ◽  
Cell Carbon

Abstract Carbon isotope fractionation during autotrophic growth o f different bacteria which possess different autotrophic CO2 fixation pathways has been studied. 13C /12C -Ratios in the cell carbon of the following bacteria were determined (CO2 fixation pathway suggested or proven in paren­theses): Alkaligenes eutrophus (reductive pentose phosphate cycle), Desulfobacterium autotrophicum and Acetobacterium woodii (reductive acetyl-CoA pathway), Desulfobacter hydrogenophilus and Thermoproteus neutrophilus (reductive citric acid cycle). The Δδ13C values, which indicate the per mille deviation of the 13C content of cell carbon from that of the CO : used as the sole carbon source, range from - 10%° (reductive citric acid cycle) over - 26%° (reductive pentose phosphate cycle) to -36%° (reductive acetyl-CoA pathway). Acetate formed via the acetyl-CoA pathway by the acetogenic Acetobacterium woodii showed a Δδ13C = -40%°. These data are discussed in view of the different CO2 fixation reactions used by the bacteria and especially with regard to the isotopic composition of sedimentary carbon through time.

scholarly journals Control of Citric Acid Cycle Activity in Rat Heart Mitochondria

1970 ◽  
Vol 245 (1) ◽  
pp. 102-111 ◽  
Author(s):  
Kathryn LaNoue ◽  
William J. Nicklas ◽  
John R. Williamson
Keyword(s):  
Citric Acid ◽  
Rat Heart ◽  
Citric Acid Cycle ◽  
Heart Mitochondria ◽  
Acid Cycle ◽  
Rat Heart Mitochondria

Differences between mouse and rat pancreatic islets: succinate responsiveness, malic enzyme, and anaplerosis

2002 ◽  
Vol 283 (2) ◽  
pp. E302-E310 ◽  
Author(s):  
Michael J. MacDonald
Keyword(s):  
Citric Acid ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Malic Enzyme ◽  
Citric Acid Cycle ◽  
Acetyl Coa ◽  
Acid Cycle ◽  
Rat Islets ◽  
Rat Pancreatic Islets ◽  
Mouse Islets

Succinic acid methyl esters are potent insulin secretagogues in rat pancreatic islets, but they do not stimulate insulin release in mouse islets. Unlike rat and human islets, mouse islets lack malic enzyme and, therefore, are unable to form pyruvate from succinate-derived malate for net synthesis of acetyl-CoA. Dimethyl-[2,3-14C]succinate is metabolized in the citric acid cycle in mouse islets to the same extent as in rat islets, indicating that endogenous acetyl-CoA condenses with oxaloacetate derived from succinate. However, without malic enzyme, the net synthesis from succinate of the citric acid cycle intermediates citrate, isocitrate, and α-ketoglutarate cannot occur. Glucose and other nutrients that augment α-ketoglutarate formation are secretagogues in mouse islets with potencies similar to those in rat islets. All cycle intermediates can be net-synthesized from α-ketoglutarate. Rotenone, an inhibitor of site I of the electron transport chain, inhibits methyl succinate-induced insulin release in rat islets even though succinate oxidation forms ATP at sites II and III of the respiratory chain. Thus generating ATP, NADH, and anaplerosis of succinyl-CoA plus the four-carbon dicarboxylic acids of the cycle and its metabolism in the citric acid cycle is insufficient for a fuel to be insulinotropic; it must additionally promote anaplerosis of α-ketoglutarate or two intermediates interconvertible with α-ketoglutarate, citrate, and isocitrate.

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