Titlebook: Glutamine in Clinical Nutrition; Rajkumar Rajendram,Victor R. Preedy,Vinood B. Pate Book 2015 Springer Science+Business Media New York 201

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https://doi.org/10.1007/978-3-322-83264-1aling system, which exists between the synaptic cells and glia cells, converts glutamine into/from glutamate in the nervous system. Large numbers of glutamate binding sites are localized in the pituitary gland. In addition, mRNA expression of many subtypes of glutamate receptors were found in periph

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https://doi.org/10.1007/978-3-7091-6934-6gen consumption. In liver, endotoxemia decreases glutamine content and mitochondrial oxygen consumption while in skeletal muscles, it increases glutamine synthesis and release resulting in decreased muscle glutamine content. In lungs, endotoxemia decreased glutamine uptake with increased glutamine s

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https://doi.org/10.1007/978-3-322-97154-8y deviate from the normal range, which is associated with an unfavorable outcome. The underlying mechanisms are still obscure. This chapter merely deals with the empirically finding of plasma glutamine concentration in humans in health and disease.

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https://doi.org/10.1007/978-3-322-95529-6or the appropriate function of many organs and the principal metabolic fuel for different rapidly dividing cells. Moreover, GLN is essential for cell metabolism because it is able to modulate gluconeogenesis, lipogenesis, anabolic processes, to preserve mitocondrial ATP levels and attenuate the acti

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https://doi.org/10.1007/978-3-663-08692-5. Fifteen patients received EN supplemented with glutamine (30 g; GLN group) for 2 d followed by EN supplemented with calcium caseinate (30 g, CAS group), also over 2 d. The other 15 patients received EN with calcium caseinate (30 g; CAS group) for 2 d followed by EN with glutamine (30 g; GLN group)