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Enzymes and associated electron transport systems that catalyse the respiratory reduction of nitrogen oxides and oxyanions. Ecological aspects of the distribution of different autotrophic CO2 fixation pathways. Muscle energetics and pulmonary oxygen uptake kinetics during moderate exercise. The genome sequence of Rickettsia prowazekii and the origin of mitochondria. (E,F) presents the relationship of flux through PK to the free energy of hydrolysis of ATP (−ΔG ATP) at cytoplasmic / values from 0.0005 to 0.015.Īndersson S. (C,D) presents the relationship of flux through PK to the calculated energy state (/ f) for cytoplasmic / values from 0.0005 to 0.015. The simulations were carried out using MatLab ((A,B) presents the relationship of flux through PK to f for cytoplasmic / values from 0.0005 to 0.015 for skeletal muscle (3A) and liver (3B). Note that is proportional to, other variables held constant, so the dependence on s not presented. was assumed to be constant at 8 μM, and was set to be near 4 mM when the / was near 2 (resting muscle). The simulated range in f (27 to 115 μM) corresponds to a range in / of 2 to 0.5. Simulations for skeletal muscle, but not liver, included equilibrium of the creatine kinase reaction. Experimental values for and Vm (Veech et al., 1979) were used: Vm = 387 and 50 μmoles/min/g wet weight and = 8and 3.4 mM for skeletal muscle and liver, respectively. The variables associated with PK (K Madp, K Mpep, and the Vm) were assumed tissue specific and constant. The simulated concentrations and rates are shown for 2 tissues, skeletal muscle (A,C,E) and liver (B,D,F). The steady state rate expression (see text equation 9). As described in the text, PK was assumed to be irreversible and to equilibrate with its substrates in a random bi bi enzyme mechanism without product inhibition. (A–F) Simulation of the relationship of flux through PK to the metabolic variables in the preceding near equilibrium reactions.
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Addition of gluconeogenesis, for example, resulted in added regulation to PK activity to prevent futile cycling PK needs to be turned off during gluconeogenesis because flux through the enzyme would waste energy (ATP), subtracting from net glucose synthesis and decreasing overall efficiency.Įnergy metabolism glycolysis metabolic homeostasis metabolic regulation pyruvate kinase. As evolution included more metabolic functions, additional layers of control were needed to integrate new functions into existing metabolism without changing the homeostatic set point. These reactions appeared in the very earliest lifeforms and are hypothesized to have established the set point for energy metabolism. The changes in ADP and PEP alter flux through PK appropriately for restoring equality of ATP production and consumption. The resulting change in /, through near equilibrium of the reactions preceding PK, alters the concentrations of ADP and phosphoenolpyruvate (PEP), the substrates for PK. Change in the rate of ATP consumption causes mismatch between use and production of ATP. Flux through the irreversible reaction, pyruvate kinase (PK), is primarily determined by the rate of ATP consumption. Thermodynamic control is illustrated using the ATP producing part of glycolysis, glyceraldehyde-3-phosphate oxidation to pyruvate. The rest of metabolism and its regulation is constrained to maintain this set point. The result is a robust homeostatic set point (-ΔG ATP) with long term (virtually unlimited) stability. (1) the concentrations of metabolic substrates for enzymes that catalyze irreversible steps and (2) the concentrations of small molecules (AMP, ADP, etc.) that regulate the activity of irreversible reactions in metabolic pathways. Thermodynamic control of metabolism is exerted through near equilibrium reactions that determine. This is important because thermodynamic parameters are stable whereas kinetic parameters are highly variable. This metabolism is based on, and regulated by, the underlying thermodynamics.
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As a result, life as we know it is based on metabolic processes that extract energy from the environment and make it available to support life (energy metabolism). Living organisms require continuous input of energy for their existence.