Titlebook: Glutamine Metabolism in Mammalian Tissues; Dieter Häussinger,Helmut Sies Conference proceedings 1984 Springer- Verlag Berlin Heidelberg 19

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https://doi.org/10.1007/978-3-662-36515-1and accelerates cellular autophagy. Most animals, including man, are faced with a surfeit of acid. The daily metabolic CO. production obligates the formation of some 15 mol of carbonic acid; normally expiration matches cellular CO. production so the H. homeostais is not threatened by this volatile a

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https://doi.org/10.1007/978-3-662-41127-8acidosis. A perplexing problem has been the observation that despite an increase in renal ammoniagenesis from glutamine known to occur in acidosis in vivo, glutamine metabolism in vitro was depressed by acid pH [1–3], probably by inhibition of phosphate-dependent glutaminase [4]. Although glutamine

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https://doi.org/10.1007/978-3-662-36521-2he only important enzyme thought to initiate renal degradation of glutamine (Tannen 1978), the main precursor of the urinary ammonia needed to serve as a buffer for excess protons (Van Slyke et al. 1943, Pitts et al. 1965), has been shown to be present in the kidney of all the species that have been

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https://doi.org/10.1007/978-3-662-00847-8igh biochemical activity which initiates production of various mediators of immunity including antibodies if they are B-lymphocytes and the mediators of cellular immunity (e.g., lymphotoxin, chemotactic factors, mitogenic factors) if they are T-lymphocytes. To perform this activity lymphocytes requi

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Enzymes of Renal Glutamine Metabolismsis (Tannen 1978, Kovacevic and McGivan 1983). The amide and amine nitrogens of glutamine are released as ammonium ions. The increased ammoniagenesis provides an expendable cation which facilitates the excretion of anions and titratable acids without depleting the body’s supply of sodium and potassi