Work Demanding High Energy Metabolism

2016 ◽  
pp. 32-71
Keyword(s):  
Energy Metabolism ◽  
High Energy

scholarly journals Energy Metabolism of Human Leukemic Lymphocytes and Granulocytes

Blood ◽  
1967 ◽  
Vol 30 (2) ◽  
pp. 151-167 ◽  
Author(s):  
JOHN LASZLO ◽  
Clarence Ellis
Keyword(s):  
Energy Metabolism ◽  
Chronic Lymphocytic Leukemia ◽  
Glucose Concentration ◽  
Acute Lymphocytic Leukemia ◽  
Aerobic Glycolysis ◽  
High Energy ◽  
Lymphocytic Leukemia ◽  
Anaerobic Conditions ◽  
High Energy Phosphate

Abstract 1. Leukocytes taken from patients having acute lymphocytic leukemia and chronic lymphocytic leukemia are characterized by high respiratory rates and low to absent aerobic glycolysis. Leukemic granulocytes have low respiratory rates and high aerobic glycolysis. 2. Lymphocytes and granulocytes have the capacity for high glycolytic rates under anaerobic conditions. 3. Lymphocyte respiration is independent of glucose concentration in contrast to granulocyte respiration. 4. High energy phosphate levels of lymphocytes and granulocytes are unchanged if these cells are incubated aerobically, either with or without glucose, or anaerobically in the presence of glucose. 5. Aerobic glycolysis can be induced in lymphocytes by the addition of foreign plasma. Foreign plasma may also alter granulocyte metabolism.

Fatty acid, tricarboxylic acid cycle metabolites, and energy metabolism in vascular smooth muscle

1994 ◽  
Vol 267 (2) ◽  
pp. H764-H769 ◽  
Author(s):  
J. T. Barron ◽  
S. J. Kopp ◽  
J. Tow ◽  
J. E. Parrillo
Keyword(s):  
Smooth Muscle ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Lactate Production ◽  
Tca Cycle ◽  
High Energy ◽  
Tricarboxylic Acid ◽  
O2 Consumption

The influence of octanoate on O2 consumption, tricarboxylic acid (TCA) cycle intermediates, and high-energy phosphates was examined in intact resting porcine carotid artery to investigate the role of fatty acid in energy metabolism and its integration with glucose metabolism in vascular smooth muscle. Incubation of resting arteries with octanoate (0.5 mM), which was previously shown to inhibit aerobic glycolysis (6), inhibited lactate production by 64% and increased O2 consumption by 30%. The increase in O2 consumption with octanoate was approximately equal to that calculated to account for the ATP production lost by inhibition of aerobic lactate production by octanoate. In glucose-free medium, the level of high-energy phosphate was reduced but was restored when octanoate was included in the incubation medium. This was associated with an increase in O2 consumption. These results suggest that the energy requirements of resting carotid artery can be largely met by the oxidative metabolism of fatty acid. Octanoate induced anaplerosis of the TCA cycle, as indicated by a 70% increase in the level of citrate. Extracellular glucose was necessary for octanoate-induced anaplerosis, probably by providing the extra carbon via pyruvate carboxylation, whereas a coupled transamination involving aspartate was a less important anaplerotic mechanism.

Impaired energy metabolism in rat myocardium during phosphate depletion

1982 ◽  
Vol 242 (6) ◽  
pp. F699-F704 ◽  
Author(s):  
N. Brautbar ◽  
R. Baczynski ◽  
C. Carpenter ◽  
S. Moser ◽  
P. Geiger ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Inorganic Phosphorus ◽  
High Energy ◽  
Deficient Diet ◽  
Myocardial Energetics ◽  
Phosphate Depletion ◽  
Myocardial Biopsies ◽  
Mitochondrial Capacity

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.

Control mechanisms in blood fluidity: role of adenosine triphosphate

1963 ◽  
Vol 18 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
L. O. Pilgeram ◽  
D. A. Loegering
Keyword(s):  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
High Energy ◽  
Control Mechanisms ◽  
High Energy Phosphate ◽  
Cellular Mechanisms ◽  
Blood Fluidity ◽  
Phosphate Linkage ◽  
Glass Surfaces

A possible role for cellular energy metabolism in the control of the blood clotting mechanism has been shown. High-energy phosphate was found to strongly inhibit the recalcification time of plasma prepared with siliconized or glass surfaces. The nucleotide, adenosine triphosphate, in crystalline form and chromatographically pure, will inhibit or completely prevent coagulation in vitro. Reactivity is based primarily on the high-energy phosphate linkage and secondarily upon the nucleoside, adenosine. The principal site of action for ATP is on an unidentified precursor of thromboplastin. Available evidence indicates an important role for energy metabolism in the cellular mechanisms which effect a control over thromboplastin generation and its possible thrombotic and arteriosclerotic sequelae. cellular control mechanisms; blood fluidity; thrombosis arteriosclerosis; aging Submitted on July 1, 1963

scholarly journals Vip1 is a kinase and pyrophosphatase switch that regulates inositol diphosphate signaling

2020 ◽  
Vol 117 (17) ◽  
pp. 9356-9364 ◽  
Author(s):  
D. Eric Dollins ◽  
Wenli Bai ◽  
Peter C. Fridy ◽  
James C. Otto ◽  
Julie L. Neubauer ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Gene Product ◽  
Active Sites ◽  
High Energy ◽  
Atomic Resolution ◽  
Cellular Adaptation ◽  
Dual Functional ◽  
Evolutionarily Conserved ◽  
Inositol Pyrophosphates ◽  
Conserved Gene

Inositol diphosphates (PP-IPs), also known as inositol pyrophosphates, are high-energy cellular signaling codes involved in nutrient and regulatory responses. We report that the evolutionarily conserved gene product, Vip1, possesses autonomous kinase and pyrophosphatase domains capable of synthesis and destruction of D-1 PP-IPs. Our studies provide atomic-resolution structures of the PP-IP products and unequivocally define that the Vip1 gene product is a highly selective 1-kinase and 1-pyrophosphatase enzyme whose activities arise through distinct active sites. Kinetic analyses of kinase and pyrophosphatase parameters are consistent with Vip1 evolving to modulate levels of 1-IP7 and 1,5-IP8. Individual perturbations in kinase and pyrophosphatase activities in cells result in differential effects on vacuolar morphology and osmotic responses. Analogous to the dual-functional key energy metabolism regulator, phosphofructokinase 2, Vip1 is a kinase and pyrophosphatase switch whose 1-PP-IP products play an important role in a cellular adaptation.

Workshop no. 1. Alternate metabolic pathways in protozoan energy metabolism

Parasitology ◽  
1981 ◽  
Vol 82 (4) ◽  
pp. 1-30 ◽  
Keyword(s):  
Energy Metabolism ◽  
Metabolic Pathways ◽  
Functional Role ◽  
High Energy ◽  
Strictly Anaerobic ◽  
Factors Affecting ◽  
Subcellular Compartmentation ◽  
Similarities And Differences ◽  
Metabolic Behaviour

The purpose of this workshop was to collect together colleagues investigating the intermediary metabolism of protozoa, with a view to discussing those pathways involved in energy metabolism and the production of ATP and other high-energy compounds, together with the factors affecting energy balance. The aspects of energy metabolism chosen for discussion comprised the metabolic pathways ranging from the strictly anaerobic to highly oxidative; subcellular compartmentation of these pathways within the protozoa; the functional role of these pathways including a consideration of aero-tolerance; and the use of inhibitors as biochemical probes and potential chemotherapeuticagents. Hopefully this approach has produced a broad 'over-view' of important areas of protozoan energy metabolism which will enable both the specialist and non-specialist to appreciate the similarities and differences between the metabolic behaviour of a range of protozoa.

scholarly journals Comparison of the Effects of Cyclosporin a on the Metabolism of Perfused Rat Brain Slices during Normoxia and Hypoxia

2002 ◽  
Vol 22 (3) ◽  
pp. 342-352 ◽  
Author(s):  
Natalie Serkova ◽  
Paul Donohoe ◽  
Sven Gottschalk ◽  
Carsten Hainz ◽  
Claus U. Niemann ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cyclosporin A ◽  
Rat Brain ◽  
Ex Vivo ◽  
Brain Slices ◽  
High Energy ◽  
Metabolic Effects ◽  
Resonance Spectroscopy ◽  
Buffer Solution ◽  
Mitochondrial Energy Metabolism

The authors evaluated and compared the metabolic effects of cyclosporin A in the rat brain during normoxia and hypoxia/reperfusion. Ex vivo31P magnetic resonance spectroscopy experiments based on perfused rat brain slices showed that under normoxic conditions, 500 μg/L cyclosporin A significantly reduced mitochondrial energy metabolism (nucleotide triphosphate, 83 ± 9% of controls; phosphocreatine, 69 ± 9%) by inhibition of the Krebs cycle (glutamate, 77 ± 5%) and oxidative phosphorylation (NAD+, 65 ± 14%) associated with an increased generation of reactive oxygen species (285 ± 78% of control). However, the same cyclosporin A concentration (500 μg/L) was found to be the most efficient concentration to inhibit the hypoxia-induced mitochondrial release of Ca2+ in primary rat hippocampal cells with cytosolic Ca2+ concentrations not significantly different from normoxic controls. Addition of 500 μg/L cyclosporin A to the perfusion medium protected high-energy phosphate metabolism (nucleotide triphosphate, 11 ± 15% of control vs. 35 ± 9% with 500 μg/L cyclosporin A) and the intracellular pH (6.2 ± 0.1 control vs. 6.6 ± 0.1 with cyclosporin A) in rat brain slices during 30 minutes of hypoxia. Results indicate that cyclosporin A simultaneously decreases and protects cell glucose and energy metabolism. Whether the overall effect was a reduction or protection of cell energy metabolism depended on the concentrations of both oxygen and cyclosporin A in the buffer solution.

THE INFLUENCE OF SYMPATHOMIMETIC AMINES, MONOAMINE OXIDASE INHIBITORS, AND ANTIHYPERTENSIVES UPON THE ENERGY METABOLISM IN THE RAT HEART

1966 ◽  
Vol 44 (4) ◽  
pp. 605-613 ◽  
Author(s):  
W. G. Hilliard ◽  
W. T. Oliver ◽  
G. R. Van Petten
Keyword(s):  
Energy Metabolism ◽  
Monoamine Oxidase ◽  
Rat Heart ◽  
Antihypertensive Drugs ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Monoamine Oxidase Inhibitors ◽  
Sympathomimetic Amines ◽  
Cardiac Energy Metabolism

This investigation was undertaken to determine the effects of three classes of catecholamine-releasing drugs on cardiac energy metabolism. The levels of adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), inorganic phosphate (IP), and phosphocreatine (CP) of the rat heart were measured. The sympathomimetic amines tyramine, ephedrine, methylamphetamine, and (+)- and (−)-amphetamine caused significant decreases in CP. Tyramine and (+)- and (−)-amphetamine also significantly depressed ATP. Of the antihypertensive drugs investigated, bretylium and guanethidine decreased the amount of CP present, and the latter compound also significantly decreased ATP. The administration of reserpine was without significant effect on cardiac high-energy phosphate levels. Among the monoamine oxidase inhibitors, tranylcypromine significantly lowered ATP and CP, whereas pheniprazine produced no significant changes. This study showed that those drugs which have been reported to release cardiac catecholamines also reduced cardiac levels of CP and ATP. The hypothesis is advanced that this effect is due to increased utilization of energy by two mechanisms: (a) stimulation of the active recapture mechanism for adrenergic neurotransmitters, and (b) the positive inotropic and chronotropic responses of the heart to the drug-released catecholamines. In either case, the observed decreases in the levels of ATP and CP in the heart are effects of sympathomimetic amines which have been heretofore unreported.

scholarly journals Expression of mitochondrial protein genes encoded by nuclear and mitochondrial genomes correlate with energy metabolism in dairy cattle

2020 ◽  
Author(s):  
Jigme Dorji ◽  
Christy J. Vander Jagt ◽  
Josie B. Garner ◽  
Leah C. Marett ◽  
Brett Mason ◽  
...  
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Dairy Cattle ◽  
Differential Gene Expression ◽  
High Energy ◽  
Over Expression ◽  
Cellular Energy ◽  
Network Analyses ◽  
Cellular Energy Metabolism ◽  
Differential Gene

Abstract Background Mutations in the mitochondrial genome have been implicated in mitochondrial disease, often characterised by impaired cellular energy metabolism. Cellular energy metabolism in mitochondria involves mitochondrial proteins (MPs) from both the nuclear ( Nu MP) and mitochondrial ( Mt MP) genomes. The expression of MP genes in tissues may be tissue specific to meet varying specific energy demands across the tissues. Currently, the characteristics of MP gene expression in tissues of dairy cattle are not well understood. In this study, we profile the expression of MP genes in 29 adult and six foetal tissues in dairy cattle using RNA sequencing and gene expression analyses: particularly differential gene expression and co-expression network analyses. Results MP genes were differentially expressed (DE; over-expressed or under-expressed) across tissues in cattle. All 29 tissues showed DE Nu MP genes in varying proportions of over-expression and under-expression. On the other hand, DE of Mt MP genes was observed in <50% of tissues and notably Mt MP genes within a tissue was either all over-expressed or all under-expressed . A high proportion of Nu MP (up to 60%) and Mt MP (up to 100%) genes were over-expressed in tissues with expected high metabolic demand; heart, skeletal muscles and tongue, and under-expressed (up to 45% of Nu MP, 77% of Mt MP genes) in tissues with expected low metabolic rates; leukocytes, thymus, and lymph nodes. These tissues also invariably had the expression of all Mt MP genes in the direction of dominant Nu MP genes expression. The Nu MP and Mt MP genes were highly co-expressed across tissues and co-expression of genes in a cluster were non-random and functionally enriched for energy generation pathways. The differential gene expression and co-expression patterns were validated in independent cow and sheep datasets. Conclusions This study demonstrated the biological interaction of MP genes from the mitochondrial and nuclear genomes and their over-expression in tissues with high energy demand. This highlights the importance of considering MP genes from both genomes in future studies related to mitochondrial functions and traits related to energy metabolism.

Myoglobin function and energy metabolism of isolated cardiac myocytes: effect of sodium nitrite

1991 ◽  
Vol 261 (4) ◽  
pp. 1-1
Author(s):  
Jeannette E. Doeller ◽  
Beatrice A. Wittenberg
Keyword(s):  
New York ◽  
Energy Metabolism ◽  
Cardiac Myocytes ◽  
Sodium Nitrite ◽  
Isolated Heart ◽  
High Energy ◽  
Heart Cells ◽  
High Energy Phosphates ◽  
Adult Rats ◽  
Isolated Cardiac Myocytes

Pages H53–H62, 1991: Jeannette E. Doeller and Beatrice A. Wittenberg. “Myoglobin function and energy metabolism of isolated cardiac myocytes: effect of sodium nitrite.” We regret that the following references were inadvertently dropped during printing. 26. Wittenberg, B. A., J. E. Doeller, R. K. Gupta, and R. L. White. Measurement of sarcolemmal permeability and intracellular pH, free magnesium, and high energy phosphates of isolated heart cells. In: Biology of Isolated Adult Cardiac Myocytes, edited by W. A. Clark, R. S. Decker, and T. K. Borg. New York: Elsevier, 1988, p. 188–130. 27. Wittenberg, B. A., and T. F. Robinson. Oxygen requirements, morphology, cell coat and membrane permeability of calcium tolerant myocytes from hearts of adult rats. Cell Tissue Res. 216: 231–251, 1981. 28. Wittenberg, B. A., and J. B. Wittenberg. Oxygen pressure gradients in isolated cardiac myocytes. J. Biol. Chem. 260: 6548–6554, 1985. 29. Wittenberg, B. A., and J. B. Wittenberg. Myoglobin-mediated oxygen delivery to mitochondria of isolated cardiac myocytes. Proc. Natl. Acad. Sci. USA 84: 7503–7607, 1987. 30. Wittenberg, B. A., and J. B. Wittenberg. Transport of oxygen in muscle. Annu. Rev. Physiol. 51: 857–878, 1989. 31. Wittenberg, B. A., J. B. Wittenberg, and P. R. B. Caldwell. Role of myoglobin in the oxygen supply to red skeletal muscle. J. Biol. Chem. 250: 9038–9043, 1975. 32. Wittenberg, J. B., and B. A. Wittenberg. Preparation of myoglobins. In: Methods of Enzymology, edited by S. P. Colowick and N. O. Kaplan. New York: Academic, 1981, vol. 76, p. 29–42. 33. Wittenberg, J. B., and B. A. Wittenberg. Mechanisms of cytoplasmic hemoglobin and myoglobin function. Annu. Reu. Biophys. Biophys. Chem. 19: 217–241, 1990.

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