Bioenergetics

Bioenergetics is a field in biochemistry and cell biology that concerns energy flow through living systems. This is an active area of biological research that includes the study of the transformation of energy in living organisms and the study of thousands of different cellular processes such as cellular respiration and the many other metabolic processes that can lead to production and utilization of energy in forms such as ATP molecules.

Overview

Bioenergetics is the part of biochemistry concerned with the energy involved in making and breaking of chemical bonds in the molecules found in biological organisms. It can also be defined as the study of energy relationships and energy transformations in living organisms.

Growth, development and metabolism are some of the central phenomena in the study of biological organisms. The role of energy is fundamental to such biological processes. The ability to harness energy from a variety of metabolic pathways is a property of all living organisms. Life is dependent on energy transformations; living organisms survive because of exchange of energy within and without.

In a living organism, chemical bonds are broken and made as part of the exchange and transformation of energy. Energy is available for work (such as mechanical work) or for other processes (such as chemical synthesis and anabolic processes in growth), when weak bonds are broken and stronger bonds are made. The production of stronger bonds allows release of usable energy.

Living organisms obtain energy from organic and inorganic materials. For example, lithotrophs can oxidize minerals such as nitrates or forms of sulfur, such as elemental sulfur, sulfites, and hydrogen sulfide to produce ATP. In photosynthesis, autotrophs can produce ATP using light energy. Heterotrophs must consume organic compounds. These are mostly carbohydrates, fats, and proteins. The amount of energy actually obtained by the organism is lower than the amount present in the food; there are losses in digestion, metabolism, and thermogenesis.^[1]

The materials are generally combined with oxygen to release energy, although some can also be oxidized anaerobically by various organisms. The bonds holding the molecules of nutrients together and in particular the bonds holding molecules of free oxygen together are relatively weak compared with the chemical bonds holding carbon dioxide and water together.^[2] The utilization of these materials is a form of slow combustion. That is why the energy content of food can be estimated with a bomb calorimeter. The materials are oxidized slowly enough that the organisms do not actually produce fire. The oxidation releases energy because stronger bonds have been formed. This net energy may evolve as heat, or some of which may be used by the organism for other purposes, such as breaking other bonds to do chemistry.

Living organisms produce ATP from energy sources via oxidative phosphorylation. The terminal phosphate bonds of ATP are relatively weak compared with the stronger bonds formed when ATP is broken down to adenosine monophosphate and phosphate and then dissolved in water. Here it is the energy of hydration that results in energy release. An organism's stockpile of ATP is used as a battery to store energy in cells, for intermediate metabolism. Utilization of chemical energy from such molecular bond rearrangement powers biological processes in every biological organism.

Types of reactions

Exergonic is a spontaneous reaction that releases energy. It is thermodynamically favored. On the course of a reaction, energy needs to be put in, this activation energy drives the reactants from a stable state to a highly energetic unstable configuration. These reactants are usually complex molecules that are broken into simpler products. The entire reaction is usually catabolic. The release of energy (called Gibbs free energy) is negative and equal to - ΔG because energy is lost from the bonds formed by the products.
Endergonic is an anabolic reaction that consumes energy. It has a positive ΔG because energy is required to break bonds.

The free energy (ΔG) gained or lost in a reaction can be calculated: ΔG = ΔH - TΔS

where G = Gibbs free energy, H = enthalpy, T = temperature, and S = entropy.

Cotransport

In August 1960, Robert K. Crane presented for the first time his discovery of the sodium-glucose cotransport as the mechanism for intestinal glucose absorption.^[3] Crane's discovery of cotransport was the first ever proposal of flux coupling in biology and was the most important event concerning carbohydrate absorption in the 20th century.^[4]^[5]

Chemiosmotic theory

One of the major triumphs of bioenergetics is Peter D. Mitchell's chemiosmotic theory of how protons in aqueous solution function in the production of ATP in cell organelles such as mitochondria.^[6] This work earned Mitchell the 1978 Nobel Prize for Chemistry. Other cellular sources of ATP such as glycolysis were understood first, but such processes for direct coupling of enzyme activity to ATP production are not the major source of useful chemical energy in most cells. Chemiosmotic coupling is the major energy producing process in most cells, being utilized in chloroplasts and several single celled organisms in addition to mitochondria.

Energy balance

Energy homeostasis is the homeostatic control of energy balance – the difference between energy obtained through food consumption and energy expenditure – in living systems.^[7]^[8]

References

^ FAO, Calculation of the Energy Content of Foods—Energy Conversion Factors
^ Schmidt-Rohr K (2015). "Why Combustions Are Always Exothermic, Yielding About 418 kJ per Mole of O₂". J. Chem. Educ. 92 (12): 2094–2099. doi:10.1021/acs.jchemed.5b00333.
^ Robert K. Crane, D. Miller and I. Bihler. "The restrictions on possible mechanisms of intestinal transport of sugars". In: Membrane Transport and Metabolism. Proceedings of a Symposium held in Prague, August 22–27, 1960. Edited by A. Kleinzeller and A. Kotyk. Czech Academy of Sciences, Prague, 1961, pp. 439-449.
^ Wright, Ernest M.; Turk, Eric (2004). "The sodium glucose cotransport family SLC5" (PDF). Pflügers Arch. 447 (5): 510–8. doi:10.1007/s00424-003-1063-6. PMID 12748858. Crane in 1961 was the first to formulate the cotransport concept to explain active transport [7]. Specifically, he proposed that the accumulation of glucose in the intestinal epithelium across the brush border membrane was coupled to downhill Na⁺
transport cross the brush border. This hypothesis was rapidly tested, refined and extended [to] encompass the active transport of a diverse range of molecules and ions into virtually every cell type.
^ Boyd, C A R (2008). "Facts, fantasies and fun in epithelial physiology". Experimental Physiology. 93 (3): 304. doi:10.1113/expphysiol.2007.037523. PMID 18192340. the insight from this time that remains in all current text books is the notion of Robert Crane published originally as an appendix to a symposium paper published in 1960 (Crane et al. 1960). The key point here was 'flux coupling', the cotransport of sodium and glucose in the apical membrane of the small intestinal epithelial cell. Half a century later this idea has turned into one of the most studied of all transporter proteins (SGLT1), the sodium–glucose cotransporter.
^ Peter Mitchell (1961). "Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism". Nature. 191 (4784): 144–8. Bibcode:1961Natur.191..144M. doi:10.1038/191144a0. PMID 13771349.
^ Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 179, 262–263. ISBN 9780071481274. Orexin neurons are regulated by peripheral mediators that carry information about energy balance, including glucose, leptin, and ghrelin. ... Accordingly, orexin plays a role in the regulation of energy homeostasis, reward, and perhaps more generally in emotion. ... The regulation of energy balance involves the exquisite coordination of food intake and energy expenditure. Experiments in the 1940s and 1950s showed that lesions of the lateral hypothalamus (LH) reduced food intake; hence, the normal role of this brain area is to stimulate feeding and decrease energy utilization. In contrast, lesions of the medial hypothalamus, especially the ventromedial nucleus (VMH) but also the PVN and dorsomedial hypothalamic nucleus (DMH), increased food intake; hence, the normal role of these regions is to suppress feeding and increase energy utilization. Yet discovery of the complex networks of neuropeptides and other neurotransmitters acting within the hypothalamus and other brain regions to regulate food intake and energy expenditure began in earnest in 1994 with the cloning of the leptin (ob, for obesity) gene. Indeed, there is now explosive interest in basic feeding mechanisms given the epidemic proportions of obesity in our society, and the increased toll of the eating disorders, anorexia nervosa and bulimia. Unfortunately, despite dramatic advances in the basic neurobiology of feeding, our understanding of the etiology of these conditions and our ability to intervene clinically remain limited.
^ Morton GJ, Meek TH, Schwartz MW (2014). "Neurobiology of food intake in health and disease". Nat. Rev. Neurosci. 15 (6): 367–378. doi:10.1038/nrn3745. PMC 4076116. PMID 24840801. However, in normal individuals, body weight and body fat content are typically quite stable over time^2,3 owing to a biological process termed 'energy homeostasis' that matches energy intake to expenditure over long periods of time. The energy homeostasis system comprises neurons in the mediobasal hypothalamus and other brain areas⁴ that are a part of a neurocircuit that regulates food intake in response to input from humoral signals that circulate at concentrations proportionate to body fat content^4-6. ... An emerging concept in the neurobiology of food intake is that neurocircuits exist that are normally inhibited, but when activated in response to emergent or stressful stimuli they can override the homeostatic control of energy balance. Understanding how these circuits interact with the energy homeostasis system is fundamental to understanding the control of food intake and may bear on the pathogenesis of disorders at both ends of the body weight spectrum.

Additional reading

Lehninger, Albert L (1971). Bioenergetics: The Molecular Basis of Biological Energy Transformations (2nd ed.). Addison-Wesley. ISBN 0-8053-6103-0.
Nicholls, David G.; Ferguson, Stuart J. (2002). Bioenergetics (3rd ed.). Academic Press. ISBN 0-12-518124-8.
Green DE, Zande HD (September 1981). "Universal energy principle of biological systems and the unity of bioenergetics". Proc. Natl. Acad. Sci. U.S.A. 78 (9): 5344–7. Bibcode:1981PNAS...78.5344G. doi:10.1073/pnas.78.9.5344. PMC 348741. PMID 6946475.

External links

The Molecular & Cellular Bioenergetics Gordon Research Conference (see).
American Society of Exercise Physiologists

[1] FAO, Calculation of the Energy Content of Foods—Energy Conversion Factors

[Schmidt-Rohr_15-2] Schmidt-Rohr K (2015). "Why Combustions Are Always Exothermic, Yielding About 418 kJ per Mole of O₂". J. Chem. Educ. 92 (12): 2094–2099. doi:10.1021/acs.jchemed.5b00333.

[3] Robert K. Crane, D. Miller and I. Bihler. "The restrictions on possible mechanisms of intestinal transport of sugars". In: Membrane Transport and Metabolism. Proceedings of a Symposium held in Prague, August 22–27, 1960. Edited by A. Kleinzeller and A. Kotyk. Czech Academy of Sciences, Prague, 1961, pp. 439-449.

[4] Wright, Ernest M.; Turk, Eric (2004). "The sodium glucose cotransport family SLC5" (PDF). Pflügers Arch. 447 (5): 510–8. doi:10.1007/s00424-003-1063-6. PMID 12748858. Crane in 1961 was the first to formulate the cotransport concept to explain active transport [7]. Specifically, he proposed that the accumulation of glucose in the intestinal epithelium across the brush border membrane was coupled to downhill Na⁺
transport cross the brush border. This hypothesis was rapidly tested, refined and extended [to] encompass the active transport of a diverse range of molecules and ions into virtually every cell type.

[5] Boyd, C A R (2008). "Facts, fantasies and fun in epithelial physiology". Experimental Physiology. 93 (3): 304. doi:10.1113/expphysiol.2007.037523. PMID 18192340. the insight from this time that remains in all current text books is the notion of Robert Crane published originally as an appendix to a symposium paper published in 1960 (Crane et al. 1960). The key point here was 'flux coupling', the cotransport of sodium and glucose in the apical membrane of the small intestinal epithelial cell. Half a century later this idea has turned into one of the most studied of all transporter proteins (SGLT1), the sodium–glucose cotransporter.

[6] Peter Mitchell (1961). "Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism". Nature. 191 (4784): 144–8. Bibcode:1961Natur.191..144M. doi:10.1038/191144a0. PMID 13771349.

[NHM-#-7] Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 179, 262–263. ISBN 9780071481274. Orexin neurons are regulated by peripheral mediators that carry information about energy balance, including glucose, leptin, and ghrelin. ... Accordingly, orexin plays a role in the regulation of energy homeostasis, reward, and perhaps more generally in emotion. ... The regulation of energy balance involves the exquisite coordination of food intake and energy expenditure. Experiments in the 1940s and 1950s showed that lesions of the lateral hypothalamus (LH) reduced food intake; hence, the normal role of this brain area is to stimulate feeding and decrease energy utilization. In contrast, lesions of the medial hypothalamus, especially the ventromedial nucleus (VMH) but also the PVN and dorsomedial hypothalamic nucleus (DMH), increased food intake; hence, the normal role of these regions is to suppress feeding and increase energy utilization. Yet discovery of the complex networks of neuropeptides and other neurotransmitters acting within the hypothalamus and other brain regions to regulate food intake and energy expenditure began in earnest in 1994 with the cloning of the leptin (ob, for obesity) gene. Indeed, there is now explosive interest in basic feeding mechanisms given the epidemic proportions of obesity in our society, and the increased toll of the eating disorders, anorexia nervosa and bulimia. Unfortunately, despite dramatic advances in the basic neurobiology of feeding, our understanding of the etiology of these conditions and our ability to intervene clinically remain limited.

[Homeostatic_control_of_energy_balance-8] Morton GJ, Meek TH, Schwartz MW (2014). "Neurobiology of food intake in health and disease". Nat. Rev. Neurosci. 15 (6): 367–378. doi:10.1038/nrn3745. PMC 4076116. PMID 24840801. However, in normal individuals, body weight and body fat content are typically quite stable over time^2,3 owing to a biological process termed 'energy homeostasis' that matches energy intake to expenditure over long periods of time. The energy homeostasis system comprises neurons in the mediobasal hypothalamus and other brain areas⁴ that are a part of a neurocircuit that regulates food intake in response to input from humoral signals that circulate at concentrations proportionate to body fat content^4-6. ... An emerging concept in the neurobiology of food intake is that neurocircuits exist that are normally inhibited, but when activated in response to emergent or stressful stimuli they can override the homeostatic control of energy balance. Understanding how these circuits interact with the energy homeostasis system is fundamental to understanding the control of food intake and may bear on the pathogenesis of disorders at both ends of the body weight spectrum.

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