scholarly journals Energy homeostasis is a conserved process: Evidence from Paracoccus denitrificans’ response to acute changes in energy demand

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0259636
Author(s):  
Raul Covian ◽  
Lanelle Edwards ◽  
Yi He ◽  
Geumsoo Kim ◽  
Carly Houghton ◽  
...  
Keyword(s):  
Energy Demand ◽  
Energy Homeostasis ◽  
Metabolic Response ◽  
Paracoccus Denitrificans ◽  
Model Organism ◽  
Fold Increase ◽  
Tca Cycle ◽  
Energy Generation ◽  
High Energy ◽  
High Energy Phosphates

Paracoccus denitrificans is a model organism for the study of oxidative phosphorylation. We demonstrate a very high respiratory capacity compared to mitochondria when normalizing to cytochrome aa3 content even in the absence of alternative terminal oxidases. To gain insight into conserved mechanisms of energy homeostasis, we characterized the metabolic response to K+ reintroduction. A rapid 3-4-fold increase in respiration occurred before substantial cellular K+ accumulation followed by a sustained increase of up to 6-fold that persisted after net K+ uptake stopped. Proton motive force (Δp) was slightly higher upon addition of K+ with ΔpH increasing and compensating for membrane potential (ΔΨ) depolarization. Blocking the F0F1-ATP synthase (Complex V) with venturicidin revealed that the initial K+-dependent respiratory activation was primarily due to K+ influx. However, the ability to sustain an increased respiration rate was partially dependent on Complex V activity. The 6-fold stimulation of respiration by K+ resulted in a small net reduction of most cytochromes, different from the pattern observed with chemical uncoupling and consistent with balanced input and utilization of reducing equivalents. Metabolomics showed increases in glycolytic and TCA cycle intermediates together with a decrease in basic amino acids, suggesting an increased nitrogen mobilization upon K+ replenishment. ATP and GTP concentrations increased after K+ addition, indicating a net increase in cellular potential energy. Thus, K+ stimulates energy generation and utilization resulting in an almost constant Δp and increased high-energy phosphates during large acute and steady state changes in respiration. The specific energy consuming processes and signaling events associated with this simultaneous activation of work and metabolism in P. denitrificans remain unknown. Nevertheless, this homeostatic behavior is very similar to that observed in mitochondria in tissues when cellular energy requirements increase. We conclude that the regulation of energy generation and utilization to maintain homeostasis is conserved across the prokaryote/eukaryote boundary.

Reduced substrate oxidation in postischemic myocardium: 13C and 31P NMR analyses

1990 ◽  
Vol 258 (5) ◽  
pp. H1357-H1365 ◽  
Author(s):  
E. D. Lewandowski ◽  
D. L. Johnston
Keyword(s):  
Steady State ◽  
31P Nmr ◽  
Tca Cycle ◽  
High Energy ◽  
Substrate Oxidation ◽  
High Energy Phosphates ◽  
Atp Content ◽  
And Control ◽  
13C And 31P Nmr ◽  
Postischemic Myocardium

13C and 31P nuclear magnetic resonance (NMR) spectra were used to assess substrate oxidation and high-energy phosphates in postischemic (PI) isolated rabbit hearts. Phosphocreatine (PCr) increased in nonischemic controls on switching from glucose perfusion to either 2.5 mM [3-13C]pyruvate (120%, n = 7) or [2-13C]acetate (114%, n = 8, P less than 0.05). ATP content, oxygen consumption (MVO2), and hemodynamics (dP/dt) were not affected by substrate availability in control or PI hearts. dP/dt was 40-60% lower in PI hearts during reperfusion after 10 min ischemia. Hearts reperfused with either pyruvate (n = 11) or acetate (n = 8) regained preischemic PCr levels within 45 s. Steady-state ATP levels were 55-70% of preischemia with pyruvate and 52-60% with acetate. Percent maximum [4-13C]glutamate signal showed reduced conversion of pyruvate to glutamate via the tricarboxylic acid (TCA) cycle at 4-min reperfusion (PI = 24 +/- 4%, means +/- SE; Control = 48 +/- 4%). The increase in 13C signal from the C-4 position of glutamate was similar to control hearts within 10.5 min. The increase in [4-13C]glutamate signal from acetate was not different between PI and control hearts. The ratio of [2-13C]Glu:[4-13C]Glu, reflecting TCA cycle activity, was reduced in PI hearts with acetate for at least 10 min (Control = 0.76 +/- 0.03; PI = 0.51 +/- 0.09) until steady state was reached. Despite rapid recovery of oxidative phosphorylation, contractility remained impaired and substrate oxidation was significantly slowed in postischemic hearts.

Anaerobic energy provision in aged skeletal muscle during tetanic stimulation

1991 ◽  
Vol 70 (4) ◽  
pp. 1787-1795 ◽  
Author(s):  
C. B. Campbell ◽  
D. R. Marsh ◽  
L. L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Energy Demand ◽  
Energy Charge ◽  
High Energy ◽  
High Energy Phosphates ◽  
Fischer 344 ◽  
Charge Potential ◽  
Anaerobic Energy ◽  
Gastrocnemius Muscles

The effect of age on skeletal muscle anaerobic energy metabolism was investigated in adult (11 mo) and aged (25 mo) Fischer 344 rats. Hindlimb skeletal muscles innervated by the sciatic nerve were stimulated to contract with trains of supramaximal impulses (100 ms, 80 Hz) at a train rate of 1 Hz for 60 s, with an occluded circulation. Soleus, plantaris, and red and white gastrocnemius (WG) were sampled from control and stimulated limbs. All muscle masses were reduced with age (9-13%). Peak isometric tensions, normalized per gram of wet muscle, were lower throughout the stimulation in the aged animals (28%). The potential for anaerobic ATP provision was unaltered with age in all muscles, because resting high-energy phosphates and glycogen contents were similar to adult values. Anaerobic ATP provision during stimulation was unaltered by aging in soleus, plantaris, and red gastrocnemius muscles. In the WG, containing mainly fast glycolytic (FG) fibers, ATP and phosphocreatine contents were depleted less in aged muscle. In situ glycogenolysis and glycolysis were 90.0 +/- 4.8 and 69.3 +/- 2.6 mumol/g dry muscle (dm) in adult WG and reduced to 62.3 +/- 6.9 and 51.5 +/- 5.5 mumol/g dm, respectively, in aged WG. Consequently, total anaerobic ATP provision was lower in aged WG (224.5 +/- 20.9 mumol/g dm) vs. adult (292.6 +/- 7.6 mumol/g dm) WG muscle. In summary, the decreased tetanic tension production in aged animals was associated with a decreased anaerobic energy production in FG fibers. Reduced high-energy phosphate use and a greater energy charge potential after stimulation suggested that the energy demand was reduced in aged FG fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Contraction- and hypoxia-stimulated glucose transport is mediated by a Ca2+-dependent mechanism in slow-twitch rat soleus muscle

2005 ◽  
Vol 288 (6) ◽  
pp. E1062-E1066 ◽  
Author(s):  
David C. Wright ◽  
Paige C. Geiger ◽  
John O. Holloszy ◽  
Dong-Ho Han
Keyword(s):  
Glucose Transport ◽  
Soleus Muscle ◽  
Fold Increase ◽  
High Energy ◽  
Muscle Contractions ◽  
High Energy Phosphates ◽  
Dependent Protein ◽  
Rat Soleus Muscle ◽  
Slow Twitch ◽  
Dependent Mechanism

Increases in contraction-stimulated glucose transport in fast-twitch rat epitrochlearis muscle are mediated by AMPK- and Ca2+/calmodulin-dependent protein kinase (CAMK)-dependent signaling pathways. However, recent studies provide evidence suggesting that contraction-stimulated glucose transport in slow-twitch skeletal muscle is mediated through an AMPK-independent pathway. The purpose of the present study was to test the hypothesis that contraction-stimulated glucose transport in rat slow-twitch soleus muscle is mediated by an AMPK-independent/Ca2+-dependent pathway. Caffeine, a sarcoplasmic reticulum (SR) Ca2+-releasing agent, at a concentration that does not cause muscle contractions or decreases in high-energy phosphates, led to an ∼2-fold increase in 2-deoxyglucose (2-DG) uptake in isolated split soleus muscles. This increase in glucose transport was prevented by the SR calcium channel blocker dantrolene and the CAMK inhibitor KN93. Conversely, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR), an AMPK activator, had no effect on 2-DG uptake in isolated split soleus muscles yet resulted in an ∼2-fold increase in the phosphorylation of AMPK and its downstream substrate acetyl-CoA carboxylase. The hypoxia-induced increase in 2-DG uptake was prevented by dantrolene and KN93, whereas hypoxia-stimulated phosphorylation of AMPK was unaltered by these agents. Tetanic muscle contractions resulted in an ∼3.5-fold increase in 2-DG uptake that was prevented by KN93, which did not prevent AMPK phosphorylation. Taken in concert, our results provide evidence that hypoxia- and contraction-stimulated glucose transport is mediated entirely through a Ca2+-dependent mechanism in rat slow-twitch muscle.

Differences in metabolic response of dog and goat latissimus dorsi muscle to chronic stimulation

1992 ◽  
Vol 73 (3) ◽  
pp. 806-811 ◽  
Author(s):  
J. F. Glatz ◽  
Y. F. de Jong ◽  
W. A. Coumans ◽  
C. M. Lucas ◽  
F. H. van der Veen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Latissimus Dorsi ◽  
Citrate Synthase ◽  
Metabolic Response ◽  
High Energy ◽  
Metabolic Adaptation ◽  
Acid Oxidation ◽  
Type I ◽  
High Energy Phosphates ◽  
Chronic Stimulation

The latissimus dorsi (LD) muscle is considered suitable to assist ventricular mechanical function in either cardiomyoplasty or extra-aortic-assist devices. Such application requires that this mixed-type skeletal muscle be transformed into a fatigue-resistant muscle, the adaptation of which can be elicited by chronic stimulation. In this study the LD muscles of dog and goat were subjected in situ to 12 wk of continuous electrical stimulation through intramuscular electrodes, and their myofibrillar and metabolic adaptations were compared. A gradual increase in the contraction rate of the muscle (in 10 wk from 30 to 80 contractions/min) caused the proportion of immunohistochemically identified type I fibers to increase in dog muscle from 30 to 74% and in goat muscle from 21 to 99%. Correspondingly, the anaerobic-glycolytic activity (fructose-6-phosphate kinase and lactate dehydrogenase activities) decreased by approximately 75% in both dog and goat muscles, whereas the oxidative capacity (fatty acid oxidation and citrate synthase activity) increased two- to threefold in goat LD muscle but remained unaltered in dog LD muscle. Muscular contents of high-energy phosphates and endogenous substrates were maintained, but the L-carnitine content decreased by 43% in both dog and goat. Our data further indicate that, for the monitoring of the metabolic adaptation of skeletal muscle, the ratio of activities of the oxidative and anaerobic-glycolytic pathways (e.g., citrate synthase to fructose-6-phosphate kinase activities) is a useful parameter in both dog and goat.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals A Little AXER ABC: ATP, BiP, and Calcium Form a Triumvirate Orchestrating Energy Homeostasis of the Endoplasmic Reticulum

Contact ◽  
2020 ◽  
Vol 3 ◽  
pp. 251525642092679
Author(s):  
Richard Zimmermann ◽  
Sven Lang
Keyword(s):  
Endoplasmic Reticulum ◽  
Energy Demand ◽  
Energy Homeostasis ◽  
Atp Synthesis ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Molecular Probes ◽  
Cellular Energy ◽  
Amp Activated Protein Kinase ◽  
Acting In Concert

Pioneering work in the 1990s started to address an interesting question. How is the main cellular energy source, adenosine triphosphate (ATP), imported into the mammalian endoplasmic reticulum (ER)? Despite its high-energy demand, large volume, and structural as well as functional complexity, the ER harbors no intricate system for ATP synthesis or regeneration. Although the original biochemical reconstitution approaches established hallmarks of the ATP transport into the ER including nucleotide selectivity, affinity, and antiport mode, the more recent live-cell imaging methods employing sensitive, localized molecular probes identified the elusive ATP/adenosine diphosphate (ADP) exchanger. According to its selectivity and localization, the identified SLC35B1 protein was rebranded AXER. Here, we discuss the identification and regulation of AXER plus the cytosolic partners (AMP-activated protein kinase, AMPK) and subcellular structures (mitochondrial–ER contact sites, MERCs) acting in concert with it to orchestrate energy homeostasis of the mammalian ER. Furthermore, we combine the two seemingly controversial regulatory mechanisms (lowER and CaATiER) in a unifying hypothesis.

scholarly journals Active Buildings Based on Passivhaus Standard to Reduce the Energy Deficit of Regional Electric Network: Proposal Analysis

Electronics ◽  
2021 ◽  
Vol 10 (19) ◽  
pp. 2361
Author(s):  
Josué Aarón López-Leyva ◽  
Carolina Barrera-Silva ◽  
Luisa Fernanda Sarmiento-Leyva ◽  
María Fernanda González-Romero
Keyword(s):  
Distributed Generation ◽  
Energy Demand ◽  
Renewable Energy Sources ◽  
Energy Generation ◽  
High Energy ◽  
Energy Deficit ◽  
Electrical Network ◽  
Net Generation ◽  
Base Case ◽  
Heating And Cooling

This manuscript presents the analysis of a real distributed generation network considering the integration of Active Buildings that meet the Passivhaus standard criteria at the Premium level, as a base case model. The novelty aspect presented in this paper is the interconnection of Active Buildings based on the Passivhaus standard at the Premium level with the National Electricity System (particularly, in Mexico’s North Baja California region) to mitigate the energy deficit. The objective of the proposal grid is to reduce the energy deficit (≈600 MW) due to the high energy demand in the region and the reduced energy generation through conventional and renewable energy sources. In a particular way, the energy rehabilitation of some buildings was analyzed with the aim of reducing the energy demand of each one and then adding energy generation through renewable sources. As a result, all Passivhaus standard criteria (i.e., heating and cooling demands, heating and cooling loads, among others) were met. Regarding the Active Buildings performance in each distributed generation circuit, an overall installed power capacity of ≈2.3 MW was obtained, which corresponds to ≈19.1% of the maximum capacity, and ≈34.30% of the recommended integration capacity. In addition, adequate results were obtained related to the import and export of energy between distributed generation circuits, i.e., the energy exchange is up to ≈106.8 kW, intending to reduce the energy contribution of the utility electrical network. Finally, the analysis of the Active Buildings showed an increase in the net generation forecast, up to ≈2.25 MW.

scholarly journals The Flux from Glucose to Glutamate in the Rat Brain in vivo as Determined by 1-Observed, 13C-Edited NMR Spectroscopy

1990 ◽  
Vol 10 (2) ◽  
pp. 170-179 ◽  
Author(s):  
Susan M. Fitzpatrick ◽  
Hoby P. Hetherington ◽  
Kevin L. Behar ◽  
Robert G. Shulman
Keyword(s):  
Steady State ◽  
Nmr Spectroscopy ◽  
Rat Brain ◽  
Tca Cycle ◽  
Difference Spectrum ◽  
Order Rate Constant ◽  
High Energy ◽  
High Energy Phosphates ◽  
Measured Intensity

The rate of incorporation of carbon from [1-13C]glucose into the [4-CH2] and [3-CH2] of cerebral glutamate was measured in the rat brain in vivo by 1H-observed, 13C-edited (POCE) nuclear magnetic resonance (NMR) spectroscopy. Spectra were acquired every 98 s during a 60-min infusion of [1-13C]glucose. Complete time courses were obtained from six animals. The measured intensity of the unresolved [4-13CH2] resonances of glutamate and glutamine increased exponentially during the infusion and attained a steady state in ∼20 min with a first-order rate constant of 0.130 ± 0.010 min−1 (t1/2 = 5.3 ± 0.5 min). The appearance of the [3-13CH2] resonance in the POCE difference spectrum lagged behind that of the [4-13CH2] resonance and had not reached steady state at the end of the 60-min infusion (t1/2 = 26.6 ± 4.1 min). The increase observed in 13C-labeled glutamate represented isotopic enrichment and was not due to a change in the total glutamate concentration. The glucose infusion did not affect the levels of high-energy phosphates or intracellular pH as determined by 31P NMR spectroscopy. Since glucose carbon is incorporated into glutamate by rapid exchange with the tricarboxylic acid (TCA) cycle intermediate α-ketoglutarate, the rate of glutamate labeling provided an estimate of TCA cycle flux. We have determined the flux of carbon through the TCA cycle to be ≈1.4 μmol g−1 min−1. These experiments demonstrate the feasibility of measuring metabolic fluxes in vivo using 13C-labeled glucose and the technique of 1H-observed, 13C-decoupled NMR spectroscopy.

Sepsis does not impair tricarboxylic acid cycle in the heart

1991 ◽  
Vol 260 (1) ◽  
pp. C50-C57 ◽  
Author(s):  
R. S. Hotchkiss ◽  
S. K. Song ◽  
J. J. Neil ◽  
R. D. Chen ◽  
J. K. Manchester ◽  
...  
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Cecal Ligation ◽  
Tca Cycle ◽  
High Energy ◽  
Tricarboxylic Acid ◽  
Female Rats ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
The Tca Cycle ◽  
Tca Cycle Intermediates

Sepsis has been reported to cause mitochondrial dysfunction and inhibition of key enzymes that regulate the tricarboxylic acid (TCA) cycle. We investigated the effect of sepsis on high-energy phosphates, glycolytic and TCA cycle intermediates, and specific amino acids that are involved in regulating the size of the TCA cycle pool during changes in metabolic state of the heart. Sepsis was induced in 12 female rats by the cecal ligation and perforation technique under halothane anesthesia; seven control rats underwent cecal manipulation without ligation. At 36-42 h postsurgery, the rats were reanesthetized, the chest was opened, and the hearts were freeze-clamped. Perchloric acid extracts of the hearts were analyzed with fluorometric enzymatic methods and 31P nuclear magnetic resonance spectroscopy. There were no significant differences in the levels of the TCA cycle intermediates or high-energy phosphates between the septic and control rats. The major metabolic changes were the 28% decrease in alanine and the 31% decrease in glutamate in the septic hearts compared with control (P less than 0.05 and P less than 0.005, respectively). Phosphocholine, a component of membrane phospholipids, was increased by 91% in the septic hearts (P less than 0.01). We conclude that sepsis does not impair the TCA cycle or induce significant cellular ischemia in the heart. The increase in phosphocholine may represent significant cellular membrane disruption during sepsis.

Transgenic livers expressing mitochondrial and cytosolic CK: mitochondrial CK modulates free ADP levels

2002 ◽  
Vol 282 (2) ◽  
pp. C338-C346 ◽  
Author(s):  
Nadir Askenasy ◽  
Alan P. Koretsky
Keyword(s):  
Atp Synthesis ◽  
Fold Increase ◽  
High Energy ◽  
High Energy Phosphates ◽  
Saturation Transfer ◽  
Reaction Velocity ◽  
Total Enzyme Activity ◽  
Phosphorus Metabolites ◽  
Total Enzyme

The function of creatine kinase (CK) and its effect on phosphorus metabolites was studied in livers of transgenic mice expressing human ubiquitous mitochondrial CK (CK-Mit) and rat brain CK (CK-B) isoenzymes and their combination.31P NMR spectroscopy and saturation transfer were recorded in livers of anesthetized mice to measure high-energy phosphates and hepatic CK activity. CK reaction velocity was related to total enzyme activity irrespective of the isoenzyme expressed, and it increased with increasing concentrations of creatine (Cr). The fluxes mediated by both isoenzymes in both directions (phosphocreatine or ATP synthesis) were equal. Over a 20-fold increase in CK-Mit activity (28–560 μmol · g wet wt−1 · min−1), the fraction of phosphorylated Cr increased 1.6-fold. Hepatic free ADP concentrations calculated by assuming equilibrium of the CK-catalyzed reaction in vivo decreased from 84 ± 9 to 38 ± 4 nmol/g wet wt. Calculated free ADP levels in mice expressing high levels of CK-B (920–1,635 μmol · g wet wt−1 · min−1) were 52 ± 6 nmol/g wet wt. Mice expressing both isoenzymes had calculated free ADP levels of 36 ± 4 nmol/g wet wt. These findings indicate that CK-Mit catalyzes its reaction equally well in both directions and can lower hepatic apparent free ADP concentrations.

Matching of vertebrate cardiac energy demand to energy metabolism

1987 ◽  
Vol 252 (5) ◽  
pp. R930-R937 ◽  
Author(s):  
W. R. Driedzic ◽  
B. D. Sidell ◽  
D. Stowe ◽  
R. Branscombe
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Carbohydrate Metabolism ◽  
Power Output ◽  
Energy Demand ◽  
Citrate Synthase ◽  
High Energy ◽  
High Energy Phosphates ◽  
Cardiac Power ◽  
Adenylate Pool

Concentrations of high-energy phosphates and activities of key enzymes of energy metabolism were assessed in hearts from species with differing levels of cardiac power output. Positive correlations were found between resting power output and the total adenylate pool and between citrate synthase activity and the total adenylate pool. Maximum in vitro activity levels of enzymes from energy metabolism were compared with calculated resting cardiac power output and maximal cardiac power output (as reflected by total oligomycin-insensitive adenosine-triphosphatase activity). Three indexes of carbohydrate metabolism (hexokinase, pyruvate kinase, and L-lactate dehydrogenase) all plateau at relatively low levels of energy demand. In contrast, enzymes required for aerobic fatty acid metabolism, (carnitine palmitoyltransferase and 3-hydroxyacyl-CoA dehydrogenase) and for tricarboxylic acid and electron transport (citrate synthase and cytochrome-c oxidase) show consistent increases as ATP demand is elevated. It appears that as capacity for power development by vertebrate hearts, increases across taxa, the elevated demand for ATP is met by expansion of fatty acid based aerobic metabolism and not carbohydrate metabolism.

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