Dietary glutamine suppresses endogenous glutamine turnover in the rat

Watford, Malcolm; Darcy-Vrillon, B; Duée, Pierre‐Henri

doi:10.1016/s0026-0495(00)91038-2

Cited by 9 publications

(6 citation statements)

References 27 publications

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“…This feedback inhibition may be relieved upon the removal of glutamine by glutaminase; however, this in turn produces ammonia and contributes to hyperammonemia. Removing glutamine by phenylacetate relieves GS inhibition, allowing for further glutamine production and ammonia removal and contributes to lowering blood ammonia 32–34. Our data suggest that OP treatment lowers ammonia systemically in ALF animals and subsequently attenuates the concentration of ammonia in the brain.…”

Section: Discussionmentioning

confidence: 64%

L-ornithine phenylacetate attenuates increased arterial and extracellular brain ammonia and prevents intracranial hypertension in pigs with acute liver failure

et al. 2009

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Hyperammonemia is a feature of acute liver failure (ALF), which is associated with increased intracranial pressure (ICP) and brain herniation. We hypothesized that a combination of L-ornithine and phenylacetate (OP) would synergistically reduce toxic levels of ammonia by (1) L-ornithine increasing glutamine production (ammonia removal) through muscle glutamine synthetase and (2) I n patients with acute liver failure (ALF) increased intracranial pressure (ICP) leads to brain herniation, which accounts for 30% of deaths. 1 Liver failure results in hyperammonemia, which leads to toxic levels of ammonia in the brain. In patients with ALF, an arterial ammonia level of Ͼ150 mol/L has been shown to correlate with severity of intracranial hypertension 2 and deaths from brain herniation. 3 More recently, ammonia levels were shown to be predictive of increased ICP 4 and changes in blood ammonia concentration determined death due to cerebral edema in patients with ALF. 5Abbreviations: ALF, acute liver failure; GS, glutamine synthetase; HE, hepatic encephalopathy; ICP, intracranial pressure; OP, L-ornithine phenylacetate. From the

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Section: Discussionmentioning

confidence: 64%

L-ornithine phenylacetate attenuates increased arterial and extracellular brain ammonia and prevents intracranial hypertension in pigs with acute liver failure

et al. 2009

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“…This could indicate that ruminants predominantly use a different proteolytic pathway under acidotic conditions or have been able to compensate for an increased anionic load via other mechanisms. Provision of exogenous glutamine and leucine to nonruminants with metabolic acidosis results in attenuation of protein degradation (Watford et al, 2000;Wilmore, 2001). It is important to establish a ruminant model and examine the influence of glutamine supplementation on proteolysis in ruminants.…”

Section: Introductionmentioning

confidence: 99%

Influence of glutamine infusion on ubiquitin, caspase-3, cathepsins L and B, and m-calpain expression in sheep with nutritionally induced metabolic acidosis1

Greenwood

AlZahal²,

Swanson³

et al. 2009

Journal of Animal Science

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Provision of AA has shown success in attenuating proteolytic activity in monogastrics suffering from metabolic acidosis. However, it is unknown whether AA supplementation can provide any beneficial effects to ruminants with nutritionally induced metabolic acidosis. The objective of the current study was to examine the effects of glutamine infusion on various protein degradation components across several tissues in sheep with induced metabolic acidosis. Sheep were assigned to a randomized complete block design with 2 x 2 factorial arrangement of treatments (n = 6 sheep/treatment) consisting of a control or acidosis diet, and receiving a saline or L-glutamine infusion. Sheep were fed diets for 10 d and slaughtered on d 11. Liver, kidney, and muscle samples were collected at slaughter and examined for relative messenger RNA (mRNA) expression of ubiquitin, C8, E2, cathepsin L, cathepsin B, caspase-3, and m-calpain, as well as protein expression of ubiquitin. Relative mRNA expression of C8 (P = 0.02), E2 (P = 0.06), and ubiquitin (P = 0.07) was less in kidney in acidotic vs. control sheep. Additionally, mRNA expression of m-calpain in kidney was greater (P = 0.01) as a result of glutamine infusion. There were no significant alterations (P > 0.10) in mRNA of any component as a result of acidosis in the liver or muscle. This study demonstrates the inability of metabolic acidosis to increase expression of the ubiquitin-mediated proteolytic pathway in skeletal muscle; however, downregulation of renal mRNA expression of these components is apparent during the induction of metabolic acidosis.

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“…This assumption is supported by a number of studies. It is evident that glutamine supplementation decreases the turnover of plasma glutamine and may correct intracellular glutamine deficiency, and so reduce the need for endogenous glutamine synthesis [58][59][60]. We demonstrated that infusion of glutamine -alone or as alanylglutamine -induces a decrease in leucine oxidation and an improvement of protein balance by a higher decrease in proteolysis than in protein synthesis in intact, endotoxemic, and irradiated rats [18,19].…”

Section: Effect Of Glutamine Administrationmentioning

confidence: 74%

Branched-chain Amino Acid Oxidation in Skeletal Muscle – Physiological and Clinical Importance of its Modulation by Reactant Availability

Holeček¹

2011

CNF

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Enhanced oxidation of branched-chain amino acids (BCAA; valine, leucine and isoleucine) in skeletal muscle is a typical metabolic alteration associated with activated synthesis of glutamine and development of muscle wasting in cachectic illness. The paper demonstrates that the rates of BCAA transamination and decarboxylation in skeletal muscle respond rapidly to changes in BCAA and glutamine availability. Enhanced BCAA availability increases BCAA oxidation and glutamine synthesis, while enhanced availability of glutamine suppresses BCAA oxidation. In physiological conditions, this enables compensation in alterations of amount and composition of food in order to keep optimal levels of BCAA and glutamine in the body. In cachectic illness, enhanced availability of BCAA (resulting mainly from activated proteolysis) and decreased availability of glutamine (resulting from its enhanced release by muscle) account significantly for activated BCAA oxidation and glutamine synthesis in muscle. The clinical importance of the opposite effect of BCAA and glutamine supplementation on BCAA oxidation in the treatment of muscle wasting disorders should be elucidated.

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Dietary glutamine suppresses endogenous glutamine turnover in the rat

Cited by 9 publications

References 27 publications

L-ornithine phenylacetate attenuates increased arterial and extracellular brain ammonia and prevents intracranial hypertension in pigs with acute liver failure

L-ornithine phenylacetate attenuates increased arterial and extracellular brain ammonia and prevents intracranial hypertension in pigs with acute liver failure

Influence of glutamine infusion on ubiquitin, caspase-3, cathepsins L and B, and m-calpain expression in sheep with nutritionally induced metabolic acidosis1

Branched-chain Amino Acid Oxidation in Skeletal Muscle – Physiological and Clinical Importance of its Modulation by Reactant Availability

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