As a step towards resolving it, we have studied the feasibility of simulating the behavior of a simple theoretical model in which all the catalysts needed for the metabolism of a system are themselves products of the metabolism itself, and in which there is a continuous loss of catalysts in unavoidable degradation reactions.

It is also robust, because it can recover from a catastrophic disappearance of a catalyst. Citation: Piedrafita G, Montero F, Morán F, Cárdenas ML, Cornish-Bowden A A Simple Self-Maintaining Metabolic System: Robustness, Autocatalysis, Bistability.

PLoS Comput Biol 6 8 : e Received: February 26, ; Accepted: June 29, ; Published: August 5, Copyright: © Piedrafita et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was partially supported by the research projects BFU and BFUC MICINN, Spain , and by the CNRS. GP acknowledges support from PhD scholarship FPU Ministry of Education, Spain.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. Several theories of life [1] — [5] coincide in the importance that they give to metabolic closure , the necessity for all of the catalysts essential for survival of an organism to be produced internally, as an organism cannot rely on any external agent for maintaining it.

The same considerations must apply to the self-maintaining systems at the origin of life [6] , [7]. Rosen [1] expressed this idea that catalysts must be produced by the system itself by saying that it must be closed to efficient causation.

These theories differ in their details, and each includes important points missing from the others. Among them the theory of M,R -system s, or metabolism—replacement systems , perhaps comes closest to a complete explanation of life, but it is usually presented in abstract terms [1] that make it difficult to relate it to any ordinary ideas of chemistry, metabolism and catalysis.

To give concrete expression to the idea of an M,R -system , and to evaluate its possible relevance to the origin of life, we proposed [8] — [10] a simple system of three interlocking cycles: a metabolic process produces a metabolite ST from external precursors S and T in a reaction catalyzed by a component STU that is itself the product of a replacement process , in which U is another external precursor.

The replacement process is necessary because STU, as a biological molecule, cannot be assumed to have an infinite lifetime, and even if it did it would be diluted by growth of the system and by other processes.

Moreover, replacement also needs a catalyst, which also needs to be replaced. To escape immediately from the implied infinite regress we proposed that replacement is catalyzed by a similar type of molecule, SU, that results from a secondary reaction catalyzed by STU,.

This system, illustrated in Fig. In our original proposal we assumed that only STU and SU were subject to unavoidable degradation see Fig.

In Fig. The reactions shown in red constitute the metabolic process, those in blue the replacement process, and in gray the replacement of the replacement catalyst.

b Expanded version of the model in which each catalyzed reaction is expanded into a cycle of three chemical reactions with explicit rate constants. Each forward rate constant refers to the reaction in the direction of the arrow, and the three degradation reactions, steps 4, 8 and 11, are assumed to be uncatalyzed and irreversible.

All rate constants are treated as constant with the values shown, apart from , and , which are varied but kept equal to one another in the range 0. The three external reactants S, T and U are assumed to have the constant concentrations shown.

All other concentrations are variable. All units are arbitrary, but they are consistent i. the same units of time and quantity of matter apply throughout and the model can be written in dimensionless form, if desired.

In addition, the numerical values assigned to the rate constants and external concentrations are also arbitrary. A controversial aspect of Rosen's analysis is his contention that a system closed to efficient causation cannot have computable models [11] — [14]. Many aspects of biological systems can, of course, be simulated in the computer, and many examples of metabolic simulation can be found in the literature, but typically these examples do not simulate systems that are closed to efficient causation.

In the recent simulation of aspartate metabolism in Arabidopsis thaliana [15] , for example, the enzymes were taken as given; their production was not simulated. We discuss this controversy elsewhere [16] and will not do so here, apart from noting that there is no obvious reason why the system illustrated in Fig.

On the contrary, it can certainly be simulated, as we shall show, with results that shed light of the conditions that need to be fulfilled by a self-maintaining system. We shall show that a simple M,R -system can be robust, capable of a recovering from the loss of most of its catalysts, and in addition has the interesting property of bistability.

As Delbrück [17] emphasized many years ago, multistability is also an important property for all but the simplest living organisms because it is essential for differentiation, an idea that has subsequently been developed by other authors [18].

Bistability can arise in systems considerably smaller and simpler [19] than the one we discuss in this paper, but we are concerned here with M,R -system s, which must be closed to efficient causation. For the system to be simulated it needs to be defined in precise numerical terms, and for doing this it is convenient to expand the catalytic processes shown in Fig.

All simulations and studies of the stability of the steady states found were done with Matlab and checked with COPASI [20] , or vice versa, and stoichiometric network analysis was done with MetaTool [21]. In the present paper all simulation is deterministic.

As we shall be supposing that the system in Fig. In effect, we assume that the overall chemical reactions degradation products, degradation products and degradation products are irreversible, that synthesis of ST in the reaction is thermodynamically favored, and that the concentrations of the external molecules S, T and U are constant, either because the quantities consumed by the system are too small to have any effect on their concentrations, or because they are buffered by external chemistry.

External constraints on a system of chemical reactions can be applied in two main ways, either with constant external concentrations or with constant input fluxes. In this model we have chosen the former approach, primarily to facilitate comparison with earlier work [8] — [10].

In this context it is important to note that organizational closure does not imply thermodynamic closure, or vice versa. In the Aristotelean terminology favored by Rosen [1] , closure to efficient causation is not the same as closure to material causation [10]. In a third type of closure, independent from both of these, an individual organism must be structurally closed, separated from other individuals by a skin or other barrier.

This aspect was given almost no attention by Rosen [1] , and we shall not discuss it further here, but it is clearly necessary, and it forms an important element of other theories of life such as autopoiesis [3]. The concentration evolution of the different metabolites in Fig. Stationary solutions of the system of Fig.

Both revealed the existence of a region with three distinct steady states, one trivial and two non-trivial. It is obvious that the system shown in Fig. Less obvious is whether it can construct itself and maintain itself indefinitely if it is seeded with a sufficient quantity of one catalyst.

This has been tested in the first instance with various values in the range 0—0. For the system cannot construct itself or maintain itself despite seeding with large or small initial concentrations of STU, and it always ends in a trivial steady state with all concentrations and all rates zero.

However, with smaller degradation rate constants it can reach either the trivial steady state or a non-trivial steady state with all concentrations and rates non-zero, i.

a self-maintaining regime. The results are summarized in Fig. For the system reached a trivial steady state with all concentrations zero, but at any it reached a non-trivial steady state with and all other concentrations and all rates non-zero.

Hence there is a none-to-all transition at this critical point, as indicated by the broken line in Fig. The model was simulated for and various values of , the initial concentration of STU, as shown, and allowed to evolve until a steady state was reached.

a For the trivial steady state was always reached, whereas for the non-trivial stable steady state was reached. b The evolution from the red point in panel a , with is shown. The behavior at very short times is illustrated in the inset. c The evolution from the blue point in panel a , with , is shown.

Note that the two insets are qualitatively very similar to one another, but the long-term trends in b and c are very different. STU is not of course the only catalytic intermediate that could be used for seeding the system, and results with each of the others, and for some pairs of intermediates, are shown in Table 1 , for two values of.

Two important points are evident in this table: first, any metabolite apart from ST or SU can be separately used to seed the system, and although the concentration of seed metabolite necessary to drive it to a non-trivial steady state varies with the seed, the steady state reached depends only on the degradation rate constants, and is independent of the identity of the seed.

We have also made simulations with various mixtures of metabolites used as seeds and these generalizations remain true. The reason why ST and SU cannot act as seed can be seen by inspection of Fig.

However, ST and SU can react with one another to give a product SUST capable of participating in additional reactions and closing all the loops. Not surprisingly therefore, the system can be seeded with a mixture of ST and SU even though neither of them is effective alone.

To verify the stability of the steady states, the Jacobian matrices were evaluated at the steady states obtained, and the eigenvectors and eigenvalues calculated.

For those conditions in which three steady states were obtained, , the trivial and one of the non-trivial solutions always have all eigenvalues with negative real parts, and thus are asymptotically stable. Obviously, they correspond to those reached by numerical integration experiments.

The additional non-trivial steady state calculated by the analytical solution of the non-linear algebraic equations has, however, one of the eigenvalues with positive real part, and is therefore an unstable steady state a saddle point , so in this region the system exhibits bistability.

Beyond the critical value, , only the trivial steady solution exists and is asymptotically stable, i. each of its eigenvalues has a negative real part. These results are summarized in the bifurcation diagram illustrated in Fig. For there is a region of bistability in which both trivial and non-trivial stable steady states are separated by an unstable steady state.

If the decay constants are increased proceeding to the right in the plot , the system remains in a non-trivial steady state until it falls abruptly to zero — the trivial steady state — exactly when leaving the bistability region. Only when approaching this condition can it experience a large jump after the appearance of small fluctuations in the concentrations.

In brief, the direction of movement determines the specific behavior: the jump is detected at when going to the left and at when going to the right.

The diagram of Fig. Once in the trivial steady state, it remains there even when the decay rate constants are decreased below the critical point. The hysteretic cycle cannot be completed unless we allow the possible appearance of trace quantities of any intermediate such as might result from external chemistry that could allow the system to recover the non-trivial steady state when close enough to the equilibrium condition.

The unstable steady state that appears in those conditions of bistability, , belongs to a separating barrier that constitutes a hypersurface limiting the attractor regions of both trivial and non-trivial stable steady states.

A planar region of the phase diagram is illustrated in Fig. Different initial conditions close enough to the separating barrier could drive the system either to one stable steady state or the other, as shown in Fig.

The calculation refers to. The point shown in green corresponds to the unstable steady state, which is contained in a barrier separating the attraction areas of the trivial steady state point shown in red and the non-trivial steady state point shown in blue.

The brown arrows represent a schematic illustration of the orbits followed in approaching the steady states. The inset illustrates schematically that the main plot is a two-dimensional slice of a multidimensional reality. Simulations were done with.

The initial concentration of ST was 6. The inset shows the time dependences at very low times, which are in the opposite directions from the long-term trends. It is clear that the system as described is capable of reaching a stable non-trivial steady state with finite fluxes and finite concentrations of all intermediates.

However, before it can be regarded as a useful model of a self-maintaining system, and thus relevant to the early stages of metabolic evolution, it needs to be shown to be capable of recovering from catastrophic loss of one or more catalysts. To test this, it was allowed to reach the non-trivial stable steady state characteristic of , and the concentrations of all forms of STU not only STU itself but also STUS, STUST and STUSU were then abruptly set to zero, the others being left at their steady-state values.

As seen in Fig. The figure shows the time evolution of the system, starting from the stable non-trivial steady state for after the concentrations of all forms of STU i. not only STU itself but also STUS, STUST and STUSU are abruptly set to zero, as indicated by the arrows at time zero leaving the others at their values in the non-trivial steady state.

As STU catalyzes two different processes synthesis both of SU and of ST , loss of STU is clearly the most stringent loss of catalyst one could consider, but for completeness we also tested the effect of loss of all forms of SU, with similar results. All of this shows that the system is highly robust, not only for infinitesimal perturbations, as tested by analysis of the Jacobian matrix, but also for large perturbations.

Unless it is perturbed to such a large extent that the separating barrier mentioned is crossed, e. below the threshold requirements listed in Table 1 for individual metabolites, but generalizable to combinations of metabolites , it always returns to the same non-trivial steady state.

It can equally resist very large increases in metabolite concentrations, for example, when ST was abruptly raised to times its steady-state value the system returned rapidly to the same steady state.

With the use of MetaTool [21] we have analyzed the structure of the model by means of an approximation to a stoichiometric analysis in the steady state. In this analysis. S, T and U are considered as external metabolites, the others being considered internal.

With the rates numbered as in Fig. Notice that the degradation rates and for the two catalysts STU and SU are in the same subsets as the corresponding replacement reactions: with , and ; but with and.

This explains how the replacement can efficiently balance the decay of each catalyst in the steady state. a The model contains five reaction subsets, consisting of reaction 1 red , reactions 2 and 3 magenta , reactions 4, 5, 6 and 7 blue , reactions 8, 9 and 10 green ; and reaction 11 gray.

b There are three elements of the basis, one consisting of reactions 1, 2, 3 and 11 and thus corresponding to the metabolic pathway, a second consisting of reactions 1, 2, 3, 4, 5, 6 and 7 , corresponding to both metabolic and replacement cycles, and the last consisting of reactions 1, 8, 9 and 10 , which is the pathway that replaces the replacement catalyst SU.

Note that elements and do not produce STU, and element produces neither SU nor ST, each of which is produced by the other two elements. Thus none of these elements is an enzyme-maintaining mode [23]. The resulting convex basis can be expressed in the following way: All three basis elements are shown schematically in Fig.

The first, , includes the reactions involved in the metabolism process, corresponds to both the metabolic and replacement cycles, and the third, , is the pathway that replaces the replacement catalyst SU. As previously shown in the subsets of reactions, the rate of decay of ST does not share the same rate with any other reaction.

However, it also is compensated as a consequence of the performance of the metabolic reactions , and , as deduced from the inspection of the first element of the convex basis.

To study the relative contributions of the basis elements to the steady-state flux distribution, , and were evaluated from the numerical integration results for different values of the degradation rate constants Fig. Log In. My Addresses. Internet Compliance. Become an Energetix Practitioner. Find an Energetix Practitioner.

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From metabolites to molecular genetics". Diabetes Care. Molecular Microbiology. Surgery Oxford. Archived from the original on 31 October Retrieved 28 August In Varki A, Cummings RD, Esko JD, Stanley P eds.

Essentials of Glycobiology 3rd ed. Cold Spring Harbor NY : Cold Spring Harbor Laboratory Press. Archived from the original on 24 February Retrieved 8 July Molecular Membrane Biology. Annual Review of Plant Physiology and Plant Molecular Biology.

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Alves R, Chaleil RA, Sternberg MJ July Journal of Molecular Biology. Wernegreen JJ December The Proceedings of the Nutrition Society. and why are they there? Current Opinion in Plant Biology.

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Penguin Press Science. Schneider EC, Sagan D Into the Cool: Energy Flow, Thermodynamics, and Life. University of Chicago Press. Lane N Oxygen: The Molecule that Made the World. USA: Oxford University Press.

Price N, Stevens L Fundamentals of Enzymology: Cell and Molecular Biology of Catalytic Proteins. Oxford University Press. ISBN X. Berg J, Tymoczko J, Stryer L Freeman and Company. Cox M, Nelson DL Palgrave Macmillan. Brock TD , Madigan MR, Martinko J, Parker J Brock's Biology of Microorganisms.

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For instance, one study found that caffeine was more effective at increasing fat burning during exercise in individuals with a less active sedentary lifestyle in comparison with trained athletes. Drinking coffee can significantly increase your metabolism and may help you lose weight if that is your goal.

They may explore underlying causes and offer you a tailored plan. Managing any condition that slows down your metabolism, like hypothyroidism , can help make other efforts more productive. Jumpstarting your metabolism may also require you to change a few habits like a nutrient-dense diet with limited processed foods, regular physical activity , and optimum sleep hygiene that allows your body to rest and recharge.

You may also avoid doing things that slow down your metabolism like restricting too many calories or not doing any strength resistance training.

Every body is different. Signs of a slow metabolism may vary individually but may include fatigue, digestive upset, not losing any weight despite your efforts, and easily gaining weight.

Only a healthcare professional may accurately assess your metabolism and the underlying causes of these symptoms. Restrictive diets may sometimes lead to a slow metabolism, among other health effects. Although for weight loss and fat burning you do want to consume fewer calories than you burn, your body still needs to get enough fuel and nutrients to perform body functions.

Instead of eating less, you may want to focus on nutritious foods and move more. Foods that boost your metabolism typically include protein such as meat, dairy, or legumes. Read more about the 12 best foods to boost your metabolism.

Learn about these and other foods you can eat before bed. To lose weight, you need to create a calorie deficit. This means you need to eat fewer calories than you burn, or better, burn more calories than you eat. You may want to focus on healthy eating habits while you consume enough calories to support your body functions.

Consider reducing processed foods, sugar and alcohol intake, and saturated fats. Resistance training and eating an adequate amount of protein can help preserve lean body mass.

Muscle growth helps you burn more calories at rest. Making small lifestyle changes and incorporating these tips into your routine can help increase your metabolism. Having a higher metabolism can help you lose weight and keep it off, if that is your goal, while also giving you more energy.

Try this today: In addition to trying the tips outlined above, you can also add more metabolism-boosting foods to your diet. Check out this article for a list of some nutritious foods that can support your metabolism.

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Health Conditions Discover Plan Connect. Nutrition Evidence Based 8 Ways That May Speed Up Your Metabolism. Medically reviewed by Marie Lorraine Johnson MS, RD, CPT — By Helen West, RD — Updated on January 11, Eat protein Do HIIT Try lifting Stand up Drink tea Eat spicy foods Sleep more Drink coffee FAQ Bottom line There are several easy and effective ways to support your metabolism, many of which involve making simple changes to your diet and lifestyle.

Eat plenty of protein at every meal. Do a high-intensity workout. Lift heavy things. Stand up more. Drink green tea or oolong tea. Eat spicy foods. Drink coffee. Frequently asked questions. The bottom line. Just one thing Try this today: In addition to trying the tips outlined above, you can also add more metabolism-boosting foods to your diet.

Was this helpful? How we reviewed this article: History. Jan 11, Written By Helen West. Medically Reviewed By Marie Lorraine Johnson MS, RD, CPT.