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Details

Autor(en) / Beteiligte
Titel
l-Arginine Metabolism Impairment in Sepsis and Diseases: Causes and Consequences
Ist Teil von
  • L-Arginine in Clinical Nutrition, 2016, p.145-158
Ort / Verlag
Switzerland: Springer International Publishing AG
Erscheinungsjahr
2016
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • Sepsis is recognized as a common cause for admission in ICUs. In general, sepsis and many diseases lead to alterations of the metabolism of amino acids (AA), among them arginine (Ventura et al. Amino Acids 39:1417–1426, 2010) more especially. Indeed, in humans, sepsis is characterized by a substantial decrease in arginine pools. This decrease of arginine concentration is usually due to a major increase of its consumption and a decrease of its endogenous production leading to the concept of “arginine deficiency” (Ventura et al. Amino Acids 39:1417–1426, 2010). Hence, in sepsis, it is generally admitted that endogenous synthesis (i.e., arginine is a non-essential amino acid) cannot meet the needs and arginine becomes a conditionally essential AA (Pribis et al. JPEN J Parenter Enteral Nutr 36:53–59, 2012). This may have important consequences. As a matter of fact, arginine is not only a component of proteins but also a molecule that can generate a number of active metabolites (Fig. 12.1): arginine may be the precursor of nitric oxide (NO, which is essential for the immune system), of ornithine (which is recognized as a polyamine precursor), or of agmatine (which is a major regulator of cell functions). Moreover, arginine is an important element in muscle energy: after reacting with glycine and methionine, it allows the formation of creatine. Finally, arginine acts as a secretagogue (such as insulin, glucagon, growth hormones, prolactin, and catecholamines) (Wu. Amino Acids 37:1–17, 2009). This could explain why the impairment of arginine homeostasis in sepsis and several diseases can contribute to pathophysiological alterations.
Sprache
Englisch
Identifikatoren
ISBN: 9783319260075, 3319260073
DOI: 10.1007/978-3-319-26009-9_12
Titel-ID: cdi_hal_primary_oai_HAL_hal_01957630v1

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