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Micronutrients and Nutraceuticals: Effects on Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Stella L. Volpe, Quentin Nichols
β-alanine is a beta amino acid, which means that the amino group is at the β-position from the carboxylate group. β-Alanine is produced in the liver and can be obtained from various protein sources (64) (Table 21.4). Exogenous β-alanine supplementation has been shown to increase the concentration of carnosine in the muscle, increasing the duration of intracellular buffering capacity (27). Improving intracellular buffering capacity can potentially increase the ability to sustain higher-intensity activities for a longer period of time, thus improving exercise performance (26). Additional information on the biochemistry of buffering and the use of β-alanine for improved exercise performance can be found in Chapter 22.
Contact and Combat Sports
Published in Datta Sourya, Debasis Bagchi, Extreme and Rare Sports, 2019
Beta-alanine, or 3-aminopropionic acid, is a naturally occurring beta-amino acid and a component of the histidine dipeptides carnosine and anserine, as well as vitamin B5 or pantothenic acid. Structurally, beta-alanine is a hybrid between the potent neurotransmitters L-glycine and GABA, which may explain why consumers often claim to experience a caffeine-like response from it. Beta-alanine is even gaining support within the scientific community for being secondarily classified as a neurotransmitter.
Nutritional Ergogenic Aids: Introduction, Definitions and Regulatory Issues
Published in Ira Wolinsky, Judy A. Driskell, Nutritional Ergogenic Aids, 2004
Ira Wolinsky, Judy A. Driskell
Taurine, a conditionally essential amino acid, is derived from diet or synthesized primarily in the brain and liver. The body synthesizes taurine from methionine and cysteine (Figure 12.4). Vitamin B6 is a critical cofactor in this pathway. It is a beta amino acid that is not utilized in protein synthesis.21
Taurine abates the liver damage induced by γ-irradiation in rats through anti-inflammatory and anti-apoptotic pathways
Published in International Journal of Radiation Biology, 2020
Engy F. El-Maraghi, Kamal I. Abdel-Fattah, Saeed M. Soliman, Wael M. El-Sayed
Taurine is a semi-essential beta-amino acid since newborn mammals have a narrow ability to synthesize taurine. Therefore, humans must rely on dietary supply for taurine from meat and sea food (Lambert et al. 2015). Taurine can be endogenously synthesized from cysteine and methionine. The capacity of endogenous taurine synthesis from sulfur amino acids is very different in different mammalian species, being high in rodents, but low in humans (Stipanuk et al. 2002). Liver is the main site of taurine biosynthesis. Since taurine is a beta-amino sulfonic acid, it is not incorporated into protein biosynthesis. Several studies revealed increased taurine excretion after exposure to high doses of IR (Tyburski et al. 2008; Christophersen 2012). Taurine was found to play several important roles in physiology, including conjugation with bile acids, osmoregulation, antioxidation, calcium homeostasis, detoxification, cell membrane stabilization, and neuromodulation (Huxtable 1992). In a previous study, taurine showed both therapeutic and prophylactic activities against aluminum-induced hepatotoxicity in mice (El-Sayed et al. 2011). Taurine was also reported to ameliorate the hepatotoxicity induced by methimazole in mice (Heidari et al. 2015). In addition, in young adults with acute lymphoblastic leukemia, taurine administration was found to decrease the risk of chemotherapy-induced hepatotoxicity and nephrotoxicity as indicated by the decline of serum bilirubin, transaminases, creatinine, and urea (Islambulchilar et al. 2015). Recently, taurine succeeded in ameliorating γ-irradiation-induced brain damage in male rats in a time-dependent manner (El-Maraghi et al. 2018).
Metabolic profiling for water-soluble metabolites in patients with schizophrenia and healthy controls in a Chinese population: A case-control study
Published in The World Journal of Biological Psychiatry, 2020
Bing Cao, Dongfang Wang, Zihang Pan, Roger S. McIntyre, Elisa Brietzke, Mehala Subramanieapillai, Yasaman Nozari, Jingyu Wang
Taurine is a sulphonated beta amino acid derivative and has neuroprotective functions as a neurotransmitter, and an inhibitory neuromodulator in the central nervous system via oxidative stress, including inhibition of glutamate-induced neurotoxicity (Koido et al. 2016). Elevated levels of taurine could lead to inhibitory dysregulation. Consistent with previous studies (Prabakaran et al. 2004; Samuelsson et al. 2013; Koido et al. 2016), our results indicated that up-regulated taurine, especially in female patients, could contribute to oxidative stress damage and the neurotransmitter disorders in schizophrenia. Furthermore, the alteration of taurine could lead to N-methyl-d-aspartate (NMDA) receptor dysfunction, which has been confirmed to play a role in the onset of psychopathological symptoms and neurocognitive dysfunction in schizophrenia. However, a clinical trial showed that taurine is protective against oxidative stress, and that treatment using taurine improves schizophrenia symptoms (O'Donnell et al. 2016). Further metabolism pathway analyses of taurine using different sexes should be performed in future studies to elucidate its role. Arginine is an important metabolite in the arginine–nitric oxide (NO) pathway, which is related to physiological processes in the central nervous system as well as inflammation (Shami et al. 1995). The reciprocal regulation between arginase and nitric oxide synthase has been demonstrated (Yanik et al. 2003). Accumulating evidence indicated that in the arginine-NO pathway, NO imbalance and decreased blood arginine concentrations are involved in the pathophysiology of schizophrenia (Yanik et al. 2003; Bernstein et al. 2005; He et al. 2012). These findings support the role of arginine as a putative diagnostic marker of schizophrenia. We proposed that substrate arginine contributed to aberrant NO metabolism (Oresic et al. 2011; He et al. 2012; Zhang et al. 2016) according to our findings and previous research results.
Still More ICD-10-CM Updates!
Published in Oncology Issues, 2018
Within the Endocrine chapter there are also grammatical revisions, as well as deletions and additions to the different subcategories. Subcategory code E72.53 has a revised definition for 2019 from hyperoxaluria to primary hyperoxaluria. Two of the disorders defined as part of code E72.8 (other specified disorders of amino-acid metabolism) were deleted and new codes were assigned to this category: E72.81 Disorders of gamma aminobutyric acid (GABA) metabolism4-Hydroxybutyric aciduriaDisorders of GABA metabolismGABA metabolic defectGABA transaminase deficiencyGABA-T deficiencyGamma-hydroxybutyric aciduriaSSADHDSuccinic semialdehyde dehydrogenase deficiencyE72.89 Other specified disorders of amino acid metabolismDisorders of beta-amino acid metabolismDisorders of gamma-glutamyl cycle