ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
(from Greek, metabole: change) Metabolism (or a METABOLIC process) is the term given to all of the chemical changes that take place inside a living organism (animal or plant). It can be broken into two opposed components: CATABOLISM (from Greek, kata: down, ballein: to throw) and ANABOLISM (from Greek, ana: up, and ballein). Catabolism (or a catabolic process) is the name given to the process of breaking down molecules (see MOLECULE) into simpler units; it releases ENERGY. Anabolism (or an anabolic process) is a process of building more complex molecules from simpler units; it consumes energy. The term METABOLITE rcfers to a chemical that is the product of metabolism: a CATABOLITE is the product of catabolism, an anabolite the product of anabolism. Very often the more general term metabolite is used when more strictly catabolite would be correct. Note that the study of metabolism is central to an understanding of biology, being a central property of living things.
Cell Biology
C.S. Sureka, C. Armpilia in Radiation Biology for Medical Physicists, 2017
Metabolism is generally divided into two basic processes. They are (1) catabolism and (2) anabolism (Figure 1.6). Catabolism (destructive metabolism) is the process of breaking up large molecules (mostly carbohydrates and fats) into more simple molecules and produces energy by the way of cellular respiration (respiration is the process of oxidizing food molecules, like glucose, to carbon dioxide and water) and heat. This energy is used as fuel for anabolism, heats the body, and enables the muscles to contract and the body to move. It also produces waste products, such as CO2 etc., which is removed from the body through the skin, kidneys, lungs, and intestines. Anabolism (constructive metabolism) is the process of building and storing large biomolecules (proteins and nucleic acids) from small molecules (amino acids and nucleotides) using the energy generated from catabolism. Hence, it supports the growth of new cells, the maintenance of body tissues, and the storage of energy for future use. Anabolic and catabolic reactions take place simultaneously in cells throughout the body so that at any given moment, some biomolecules are being synthesized while others are being broken down. The energy released from or stored in the chemical bonds of biomolecules during metabolism is commonly measured in kilocalories (kcal).
The Internal Milieu Brain and Body
Rolland S. Parker in Concussive Brain Trauma, 2016
Victims of accidents causing TBI frequently report changes of weight, fatigue, loss of stamina, depression, and oversensitivity to heat and/or cold. Dysregulation of metabolism may be considered a contributor. Metabolism is the transformation of substances to provide energy, the synthesis of proteins for growth and repair. The breakdown of large molecules is catabolism, and the synthesis of large molecules from smaller ones is anabolism. Since hormones alter the way foodstuffs are utilized, they may alter the metabolic rate. Participating are catecholamines (adrenal medulla and SNS), thyroid, growth and male sex hormones, and female gonadal steroids. Hypothyroidism produces reduced tolerance to cold; increased thyroid secretion may cause the patient to feel hot (Pocock & Richards, 2004, pp. 574–575). Involved are both intracellular relationships and transfer between organs (e.g., energy transfer between adipose tissue to liver to muscles and back).
Nicotinamide protects against skeletal muscle atrophy in streptozotocin-induced diabetic mice
Published in Archives of Physiology and Biochemistry, 2019
Shizhe Guo, Qingyan Chen, Yaying Sun, Jiwu Chen
Muscle atrophy is the consequence of the disrupted homeostasis of protein anabolism and catabolism. It is well-acknowledged that two E3 ubiquitin ligases, i.e., muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx)/Atrogin1, are primarily responsible for muscle atrophy by mediating protein degradation, making them ideal biomarkers in atrophic muscle (Bodine et al., 2001, McFarlane et al., 2006, Mendias et al., 2012b). These two ligases are subjected to the regulation of transforming growth factor beta (TGF-β) pathway which is over-activated in the diabetic muscle (Mendias et al., 2012a, Ohsawa et al., 2012, Abrigo et al., 2016). However, this degradative effect is antagonized by PI3K/Akt signalling (Sun et al., 2018a). Akt activation not only down-regulates the expression of MuRF1 and Atrogin1 but facilitate protein synthesis as well (Gorgens et al., 2013).
Chinese herbal decoction (Danggui Buxue Tang) supplementation augments physical performance and facilitates physiological adaptations in swimming rats
Published in Pharmaceutical Biology, 2020
William Chih-Wei Chang, Ching-Chi Yen, Chao-Pei Cheng, Yu-Tse Wu, Mei-Chich Hsu
There are several major mechanisms involved in the effects of supplements or drugs that may augment physical performance. Boosting anabolism can result in increased muscle mass and muscular strength (Willoughby et al. 2007); stimulating activity of the central nervous system can elevate heart rate and blood pressure and reduce tiredness and fatigue (Avois et al. 2006); regulating fuel metabolism can improve exercise capacity and prolong duration until exhaustion (Ormsbee et al. 2014). Although both animal and human studies have highlighted a dramatic improvement in performance after DBT supplementation (Liu et al. 2011; Chang et al. 2018), its action in terms of biochemical regulation is not yet well understood. According to a recent metabolomics research (Miao et al. 2018), five major metabolic pathways were involved in DBT supplementation on fatigued mice: (1) phenylalanine, tyrosine and tryptophan metabolism, (2) glycine, serine, and threonine metabolism, (3) glyoxylate and dicarboxylate metabolism, (4) pyruvate metabolism, and (5) the Krebs cycle. Consequently, we deduce that DBT more likely alters the energy expenditure during exercise.
Hypothesis of using albumin to improve drug efficacy in cancers accompanied by hypoalbuminemia
Published in Xenobiotica, 2021
Soghra Bagheri, Ali A. Saboury
Drug resistance is the main cause of more than 90% of cancer patients' deaths, which its mechanism includes increasing drug metabolism, altering drug transport (increasing drug efflux/decreasing drug influx), enhancing DNA repair capacity, growth factors, and genetic factors (Bukowski et al. 2020; Zahreddine and Borden 2013). Drug metabolism does not refer to the usual metabolic pathways that include anabolism and catabolism, but rather changes that facilitate the excretion of the drug from the body (Benet and Zia-Amirhosseini 1995). There are two main phases in drug metabolism. The first phase involves processes such as oxidation, reduction, and hydrolysis that alter the pharmacological activity of the drug, usually resulting in loss of activity, and the second phase increases its solubility in water by adding endogenous molecules to the drug (Caira and Ionescu 2005). Most drugs lose their medicinal properties in this way and produce highly soluble metabolites that are easily excreted (Li et al. 2019). The main organ that metabolizes drugs is the liver. However, other organs, such as the kidneys, lungs, intestine, and skin, also have metabolizing enzymes (Alfarouk et al. 2015). Understanding drug resistance mechanisms is critical to overcoming them in order to develop new effective treatment strategies.
Related Knowledge Centers
- Biosynthesis
- Cellular Respiration
- Cofactor
- Macromolecule
- Metabolic Pathway
- Molecule
- Metabolism
- Catabolism
- Atp Hydrolysis
- Redox