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Single Amino Acids
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Proteins are composed of amino acids linked together into discrete chains. Peptides are short chains of amino acids (2 to 20 amino acid residues). Amino acids are the precursors and raw materials for proteins, peptides, nucleotides, and parts of phospholipids. Amino acid metabolism encompasses and directly impacts almost every aspect of cellular function. Pools of individual amino acids exist inside of cells, in plasma, and in other extracellular fluids. Amino acids are ubiquitous in the human body. This chapter will explore the use of individual amino acids for enhancement of musculoskeletal healing. The range of studies is from enhanced absorption of minerals to pharmacological pain control, illustrating the enormous breadth of functions for amino acids. One caveat must be considered about single amino acids, or, for that matter, any single nutrient. The human metabolism and the healing response is a complex, dynamic system with numerous homeostatic controls. Simply adding one ingredient to a complex system may or may not accentuate the desired result, or it may have unforeseen consequences. In other words, adding a single nutrient to metabolism and expecting it to exert measurable effects on the net outcome is an uphill climb. Nevertheless, with the widespread availability of pure, individual amino acids, a considerable literature has accumulated on the effects of single amino acids on musculoskeletal healing.
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Many diseases of inborn errors of metabolism are associated with aminoaciduria.297 The disorder may be primarily related to (1) enzyme defects in the intermediary metabolism or transport of amino acids such as phenylketonuria and Hartnup disease; (2) secondary interference with hepatic or renal metabolism causes by the action of an endogenous or exogenous substance, resulting in overflow and elimination of excess amino acids such as Wilson’s disease; or (3) the consequence of heavy metal poisoning. Excess tissue levels of a given amino acid may inhibit the transport of other amino acids into the brain and their utilization for protein synthesis.46,47 Respiration, synthesis of neurotransmitter substances, and myelination may also be affected. Some amino acids serve as neurotransmitters,48 implying that altered tissue levels may cause derangement in the neuronal network function.49 In some cases, the plasma level of an amino acid is elevated, and due to overflow, it appears in theurine. In others, the plasma level is low. In some diseases the anomaly of amino acid metabolism caused by an enzyme defect does not appear as accumulation in the plasma, since there is no renal mechanism for its reabsorption. Such amino acids are normally present within the cell and due to the no-threshold level they are eliminated in the urine, such as cystathionine and argininosuccinic acid. A large number of the genetic disorders of amino acid metabolism are coupled with neurologic symptoms, most commonly with mental retardation.472
Accident and Emergency
Published in Nagi Giumma Barakat, Get Through, 2006
E.Abnormal results from newborn screening The following are false regarding investigating amino acid metabolism except:
Therapeutic perspectives on the metabolism of lymphocytes in patients with rheumatoid arthritis and systemic lupus erythematosus
Published in Expert Review of Clinical Immunology, 2021
Amino acid metabolism plays an important role in immune cell activation, differentiation, and function. Amino acids are required not only for protein synthesis, but also for various cellular processes underlying inflammation, such as nucleic acid synthesis, regulation of mTORC1 signaling, and control of stress pathways [39,40]. Glutamine is a non-essential amino acid abundant in the circulatory system whose consumption is increased in activated T cells [28]. In glutaminolysis, glutamine is first hydrolyzed to glutamate and then to α-ketoglutarate which is an intermediate in the TCA cycle and a substrate for histone demethylases and DNA demethylases [41]. Glutamine deficiency [2,42] or inhibition of α-ketoglutarate [43] promotes Treg cell differentiation. Glutaminase, the first enzyme in the glutaminolytic pathway, is transcriptionally induced by ICER to promote Th17 cell differentiation. Inhibition of glutaminase suppresses Th17 cell differentiation, promotes Th1 cell differentiation, and has no effect on Treg cell differentiation [44].
Altered gut bacterial and metabolic signatures and their interaction in gestational diabetes mellitus
Published in Gut Microbes, 2020
Xing Wang, Hongli Liu, Yifan Li, Shuai Huang, Lan Zhang, Chiying Cao, Philip N. Baker, Chao Tong, Peng Zheng, Hongbo Qi
To explore potential reciprocal interactions between altered gut bacteria, fecal and urine metabolites, and glucose values, a co-occurrence network was constructed based on Spearman correlation analysis. We found that bacterial OTUs from the Enterobacteriaceae and Lachnospiraceae families formed strong co-occurring relationships with fecal and urine metabolites involved with carbohydrate and amino acid metabolism (Figure 5). The metabolites involved with carbohydrate metabolism were also strongly correlated with those related to amino acid metabolism. For example, Trehalose, which was broadly correlated with carbohydrate and amino acid metabolites, was a vital node between the two metabolic pathways within this co-expression network. Other metabolites, and bacterial Lachnospiraceae_OTU247, were correlated with FBG at 12 weeks’ gestation or OGTT blood glucose at 24–28 weeks’ gestation. These findings suggest that altered gut microbes and host metabolites formed a synergistic and nodal co-occurrence network in GDM (Figure 5).
The potential for metabolomics in the study and treatment of major depressive disorder and related conditions
Published in Expert Review of Proteomics, 2020
The potential applications of metabolomics to MDD include the disease diagnosis, treatment, and prognosis and the identification of related biomarkers. In this review, we summarized the evidence from both animal models and human patents to illustrate the roles played by metabolomics in MDD. The results from both animal models and MDD patients showed that metabolic disturbances are primarily associated with amino acid metabolism (especially neurotransmitters), energy metabolism, and lipid metabolism. Based on these results, the use of metabolites to distinguish between different groups or to evaluate treatment responses may be challenging because the identities and quantities of metabolite differences were not exactly the same between studies, although there was some overlap [22,41]. Determining how to compare and associate these varying results, based on samples collected from independent research teams using different methods and samples, is a major challenge for the future application of metabolomics to MDD. To overcome this challenge, shifting the focus from relative concentrations of metabolites to absolute metabolite concentrations has been suggested. Inter-laboratory reproducibility is another potential method for achieving comparable metabolomics results that can be applied to MDD. Untargeted metabolomics can be used to identify several specific metabolites, and resulting data can be transmitted to an independent laboratory to verify the reproducibility of the data, using similar procedures in an inter-laboratory comparison exercise.