Macronutrientst, Micronutrients, and Metabolism
Emily Crews Splane, Neil E. Rowland, Anaya Mitra in Psychology of Eating, 2019
Bioenergetics is defined as the study of the transformation of energy in living organisms. Macronutrients are energy-yielding molecules in food that fuel the citric acid cycle and generate adenosine triphosphate. The energy density of a food is its energy yield per unit weight of food and depends on the relative amounts of the three macronutrients present in that food. The globally common condition of lactose intolerance, symptoms of which include diarrhea and bloating, occurs because the enzyme that breaks lactose apart is not present after infancy. In addition to energy-yielding macronutrients, a relatively large number of non-energetic dietary components are essential constituents for the structure and function of our bodies. Metabolism is a complex physiological science, and what follows is a very simplified presentation of some essentials. The aspect that ties all of these various food classes together is that they are composed of macronutrients that supply our bodies with the energy to function.
Metabolism, nutrition, exercise and temperature regulation
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
Cells need energy for work including muscle contraction, biosynthesis, active transport across membranes and generation of heat. Energy is generated from metabolic fuels and from reduced molecules, which are oxidized to release energy. Oxidation involves removing electrons at high potential from the fuel molecules and transferring them to a lower potential, thus releasing energy. The removed electrons must be transferred to a suitable electron acceptor, which has to be transportable, soluble in water and generally available. Oxygen is not used until the end of the electron transport chain. The basic chemical currency of energy in all living cells consists of the two high-energy phosphate bonds contained in adenosine triphosphate (ATP). The immediate source of cellular energy is ATP, which can lose one phosphate group producing adenosine diphosphate and usable energy. The end product of glycolysis is pyruvate, which under aerobic conditions enters the citric acid cycle.
Metabolism
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
Gluconeogenesis is an important metabolic process by which glucose is synthesized from non-carbohydrate precursors derived from fat and protein metabolism, for example, lactate, pyruvate, glycerol and amino acids. Glycogen is synthesized from glucose when excess glucose is available, and this requires the enzyme glycogen synthase. Free fatty acid synthesis occurs mainly in the liver and adipose tissue. In the liver, the main precursor for fatty acid synthesis is endogenous glucose derived from glycogen, lactate and blood glucose. The processes of glycolysis, the citric acid cycle and the electron transport chain are described to show how they relate to cellular energy production. The citric acid cycle is an important aerobic metabolic reaction within mitochondria as it provides reduced coenzymes required for the final phase, oxidative phosphorylation. The production of ketoacids results from an imbalance between the flow of fatty acids into mitochondria of hepatocytes and the capacity of the citric acid cycle to remove acetyl coenzyme A.
Biotin Stores in Rodent Lungs: Localization to Clara and Type II Alveolar Cells
Published in Experimental Lung Research, 1988
Biotin is a cofactor for carboxylases used in fatty acid synthesis, gluconeogenesis, and energy production by the citric acid cycle. Although lung has low levels of this vitamin overall, high concentrations were demonstrated histochemically in Clara cells of mouse, rat, hamster, and guinea pig using avidin conjugated to peroxidase. Lesser concentrations were found in type II cells of mouse, rat, and hamster but not guinea pig. By electron microscopy, biotin stores in mouse Clara cells were localized to mitochondria, while those in type II cells were present in both mitochondria and the cytoplasmic matrix. Biotin stores in type II cells are probably used mainly in fatty acid synthesis but also in gluconeogenesis and energy production. The reason for particularly high concentrations in the mitochondria of Clara cells is unknown.
Enteric short-chain fatty acids: microbial messengers of metabolism, mitochondria, and mind: implications in autism spectrum disorders
Published in Microbial Ecology in Health and Disease, 2015
Clinical observations suggest that gut and dietary factors transiently worsen and, in some cases, appear to improve behavioral symptoms in a subset of persons with autism spectrum disorders (ASDs), but the reason for this is unclear. Emerging evidence suggests ASDs are a family of systemic disorders of altered immunity, metabolism, and gene expression. Pre- or perinatal infection, hospitalization, or early antibiotic exposure, which may alter gut microbiota, have been suggested as potential risk factors for ASD. Can a common environmental agent link these disparate findings? This review outlines basic science and clinical evidence that enteric short-chain fatty acids (SCFAs), present in diet and also produced by opportunistic gut bacteria following fermentation of dietary carbohydrates, may be environmental triggers in ASD. Of note, propionic acid, a major SCFA produced by ASD-associated gastrointestinal bacteria (clostridia, bacteroides, desulfovibrio) and also a common food preservative, can produce reversible behavioral, electrographic, neuroinflammatory, metabolic, and epigenetic changes closely resembling those found in ASD when administered to rodents. Major effects of these SCFAs may be through the alteration of mitochondrial function via the citric acid cycle and carnitine metabolism, or the epigenetic modulation of ASD-associated genes, which may be useful clinical biomarkers. It discusses the hypothesis that ASDs are produced by pre- or post-natal alterations in intestinal microbiota in sensitive sub-populations, which may have major implications in ASD cause, diagnosis, prevention, and treatment.
Oxidative modification of citrate synthase by peroxyl radicals and protection with novel antioxidants
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2009
Nikolai L. Chepelev, Joshua D. Bennitz, James S. Wright, Jeffrey C. Smith, William G. Willmore
In mammals, aging is linked to a decline in the activity of citrate synthase (CS; E.C. 2.3.3.1), the first enzyme of the citric acid cycle. We used 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH), a water-soluble generator of peroxyl and alkoxyl radicals, to investigate the susceptibility of CS to oxidative damage. Treatment of isolated mitochondria with AAPH for 8–24 h led to CS inactivation; however, the activity of aconitase, a mitochondrial enzyme routinely used as an oxidative stress marker, was unaffected. In addition to enzyme inactivation, AAPH treatment of purified CS resulted in dityrosine formation, increased protein surface hydrophobicity, and loss of tryptophan fluorescence. Propyl gallate, 1,8-naphthalenediol, 2,3-naphthalenediol, ascorbic acid, glutathione, and oxaloacetate protected CS from AAPH-mediated inactivation, with IC50 values of 9, 14, 34, 37, 150, and 160 μM, respectively. Surprisingly, the antioxidant epigallocatechin gallate offered no protection against AAPH, but instead caused CS inactivation. Our results suggest that the current practice of using the enzymatic activity of CS as an index of mitochondrial abundance and the use of aconitase activity as an oxidative stress marker may be inappropriate, especially in oxidative stress-related studies, during which alkyl peroxyl and alkoxyl radicals can be generated.
Related Knowledge Centers
- Carbon Dioxide
- Energy Metabolism
- Fatty Acids
- Glucose
- Biochemical Phenomena
- Metabolic Networks & Pathways
- Amino Acids