The effect of glutamine-enriched TPN on gut immune cellularity

Alverdy, John; Aoys, Eric; Weisscarrington, P; Burke, David

doi:10.1016/0022-4804(92)90275-5

Cited by 136 publications

(38 citation statements)

References 10 publications

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“…This may be due to the passage of viable bacteria through paracellular pathways, as a consequence of altered tight junction selectivity secondary to severely impaired metabolism. None of the supplements had any significant preventive effect on bacterial translocation, which is at variance with some other reports in enterally [1] or parenterally fed rats supplemented with glutamine [19] . This lack of preventive effect may be due to the fact that other factors involved in gut barrier function, such as mucosal immune cells or IgA secretion, had been impaired by severe protein restriction [1,19] .…”

Section: Discussioncontrasting

confidence: 57%

“…None of the supplements had any significant preventive effect on bacterial translocation, which is at variance with some other reports in enterally [1] or parenterally fed rats supplemented with glutamine [19] . This lack of preventive effect may be due to the fact that other factors involved in gut barrier function, such as mucosal immune cells or IgA secretion, had been impaired by severe protein restriction [1,19] . Glutathione plays an important role in detoxification reactions with xenobiotics and oxygen radicals [3] and is also required in large amounts in catabolic states, not only by hepatic and intestinal cells but also by inflammatory cells; thus, impaired mucosal glutathione content increases the susceptibility to oxidative tissue injury [3,5] .…”

Section: Discussioncontrasting

confidence: 57%

“…Glutamine supplementation may prevent gut mucosal damage and bacterial translocation in various experimental models of gut injury [13,17] . Moreover, glutamine could with stand systemic [18] but also gut-associated [19,20] immune response, because glutamine is an important substrate for optimal lymphocyte [21] and macrophage [22] function. In addition, some reports indicate that glutamine may counteract glutathione depletion by supporting gut glutathione biosynthesis [23] and may influence cytokines production by gut mucosa in rats [24] or in humans [25,26] .…”

Section: Introductionmentioning

confidence: 99%

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Effects of glutamine supplementation on gut barrier, glutathione content and acute phase response in malnourished rats during inflammatory shock

Belmonte¹,

Coëffier²,

Pessot³

et al. 2007

WJG

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AIM:To evaluate the effect of glutamine on intestinal mucosa integrity, glutathione stores and acute phase response in protein-depleted rats during an inflammatory shock. METHODS:Plasma acute phase proteins (APP), jejunal APP mRNA levels, liver and jejunal glutathione concentrations were measured before and one, three and seven days after turpentine injection in 4 groups of control, protein-restricted, protein-restricted rats supplemented with glutamine or protein powder. Bacterial translocation in mesenteric lymph nodes and intestinal morphology were also assessed. RESULTS:Protein deprivation and turpentine injection significantly reduced jejunal villus height, and crypt depths. Mucosal glutathione concentration significantly decreased in protein-restricted rats. Before turpentine oil, glutamine supplementation restored villus heights and glutathione concentration (3.24 ± 1.05 vs 1.72 ± 0.46 µmol/g tissue, P < 0.05) in the jejunum, whereas in the liver glutathione remained low. Glutamine markedly increased jejunal α1-acid glycoprotein mRNA level after turpentine oil but did not affect its plasma concentration. Bacterial translocation in protein-restricted rats was not prevented by glutamine or protein powder supplementation. CONCLUSION:Glutamine restored gut glutathione stores and villus heights in malnourished rats but had no preventive effect on bacterial translocation in our model.

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Section: Discussioncontrasting

confidence: 57%

Section: Discussioncontrasting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

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Effects of glutamine supplementation on gut barrier, glutathione content and acute phase response in malnourished rats during inflammatory shock

Belmonte¹,

Coëffier²,

Pessot³

et al. 2007

WJG

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“…It is possible, however, that the lack of specific nutrients such as glutamine, not currently included in TPN regimens, may influence immune function. 21,22 Impairment of the host defenses directly by the TPN solution has been suggested as an important factor in the high rate of TPN-associated infections. Previous studies in human adults have shown that the administration of lipid emulsions containing long-chain fatty acids results in a depletion in the host defense mechanisms, particularly in neutrophil bactericidal activity and migration.…”

Section: Discussionmentioning

confidence: 99%

Bactericidal Activity Against Coagulase-Negative Staphylococci Is Impaired in Infants Receiving Long-Term Parenteral Nutrition

Okada

Klein²,

Saene³

et al. 2000

Annals of Surgery

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ObjectiveTo examine the role of total parenteral nutrition (TPN) in predisposing infants to infection caused by coagulase-negative staphylococci. Summary Background DataTotal parenteral nutrition is an important means of providing essential nutrients to newborn infants. However, its use has been associated with complications, particularly infection caused by coagulase-negative staphylococci. Recent data suggest that TPN may modulate immune function; however, reports directly indicating impaired immunity against coagulase-negative staphylococci during TPN are limited. MethodsStudy 1 involved 31 infants younger than 4 months who had undergone surgery and were not receiving antibiotics; 20 were receiving TPN and 11 were receiving a normal enteral diet. An in vitro whole blood model was used to measure the host bactericidal activity against coagulase-negative staphylococci. Bacterial killing and phagocytosis were measured after a 45-minute challenge with viable coagulase-negative staphylococci. In study 2, whole blood killing and intracellular killing of coagulase-negative staphylococci were measured in five newborn infants (younger than 2 months) who were receiving long-term TPN (Ͼ10 days), five control infants receiving a normal enteral diet, and five healthy adults. ResultsIn study 1, infants receiving a normal enteral diet showed a high capacity to ingest and kill coagulase-negative staphylococci. In contrast, the blood of infants receiving long-term TPN showed a reduction in coagulase-negative staphylococci phagocytosis and killing. There were significant negative linear correlations between the duration of TPN and killing of coagulase-negative staphylococci and phagocytosis of coagulasenegative staphylococci. In study 2, infants receiving long-term TPN had lower whole blood killing and intracellular killing than infants receiving a normal enteral diet and healthy adult volunteers. These data seem to indicate a neutrophil dysfunction mediated by TPN in infancy. ConclusionsHost defense mechanisms, including phagocytosis and killing of coagulase-negative staphylococci, are impaired during long-term TPN. The impaired bactericidal activity seems to be related to defective intracellular killing in neutrophils. These findings may explain the high rate of septicemia caused by coagulase-negative staphylococci in infants receiving TPN.Total parenteral nutrition (TPN) has contributed to the recent improvement in the care of newborn infants. However, this form of nutritional support is associated with complications, particularly infection. Five percent to 37% of infants receiving TPN become bacteremic, 1-3 most frequently with coagulase-negative staphylococci.4 Infection may result in impairment of liver function or systemic inflammatory response syndrome, necessitating the removal of central venous catheters. It therefore represents a major clinical problem of TPN in infancy.It is generally believed that infection with coagulasenegative staphylococci results from contamination of in-

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“…Several methods for preventing such hepatic dysfunction have been reported, such as the use of cyclic TPN 13) or the administration of ursodeoxycholic acid, 14) metronidazole, 15) gentamicin, 16) anti-TNF antibody, 17) cholecystokinin, 18,19) glutamine, [20][21][22][23] or steroids and growth hormone. Nevertheless, the problem of hepatic dysfunction in patients receiving TPN has yet to be completely overcome, and the mechanism of TPN-induced hepatic steatosis remains unclear.…”

Section: Role Of Soybean Oil Fat Emulsion In the Pre-vention Of Tpn-imentioning

confidence: 99%

Soybean Oil Fat Emulsion to Prevent TPN-Induced Liver Damage: Possible Molecular Mechanisms and Clinical Implications

Nishimura

Yamaguchi

Naito

et al. 2006

Biological & Pharmaceutical Bulletin

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INTRODUCTIONTotal parenteral nutrition (TPN), which is recognized as one method for parenteral hyperalimentation, has been found to be an effective and relatively safe method for supplying energy and nutrients to surgical patients. Following improvements in parenteral regimens including vitamins and trace elements and in catheter techniques to reduce the septic complications associated with TPN, TPN has been widely employed to provide complete nutritional support and therapeutic benefits in a variety of pathophysiological settings in which patients are unable to eat. However, TPN-induced hepatobiliary dysfunction, which was first described by Peden et al.,1) has been recognized as a cause of severe morbidity and a life-threatening complication of TPN, especially in neonates and infants. Hepatic dysfunction with steatosis is the most common complication associated with fat-free TPN in adults, and cholestasis is more common in infants.2,3) Recently, the 3-component infusion solution containing amino acids, glucose, and soybean oil emulsion, GA-1080 (MIXID ® , Otsuka Pharmaceutical Factory, Inc.; Tokushima, Japan), has been demonstrated to be effective in overcoming such hepatic morbidity in clinical studies.4) Intravenous fat emulsions, especially soybean oil, are now available as a source of essential fatty acids in patients receiving TPN, and the "three-in-one" solution GA-1080 has been found to be clinically safe, stable, and economical. However, the multifactorial pathogenesis of TPN-induced hepatic dysfunction remains unclear, and the molecular mechanisms by which GA-1080 prevents hepatic dysfunction have not yet been identified.We have recently developed an infant rat model of hepatobiliary dysfunction.5) Using this animal model, we have clearly demonstrated the metabolic complications in the liver that may occur due to the excessive administration of fat-free TPN in infant rats. Furthermore, we have shown that including fat in the TPN regimen is very important in preventing TPN-induced hepatic dysfunction. In this review, we describe the molecular mechanisms and the clinical implications of soybean oil in TPN solutions in avoiding the hepatic complications associated with parenteral nutrition. INFANT RAT TPN MODEL WITH HEPATOBILIARY DYSFUNCTIONSince the first studies of TPN in animal models conducted in 1968 by Dudrick et al.,6) it has been known that only a limited number of species (such as the dog, cat, rabbit, and guinea pig) can tolerate the surgical procedures required for TPN, and few studies have employed rats as an animal model for TPN. In 1981, Tashiro and Meng 7) were the first to report a technique for long-term TPN in unrestrained weanling or infant (3-week-old) rats, thus establishing an animal model for pediatric TPN. Numerous studies have focused on the optimal TPN composition in mature rats, but few have addressed this issue in infant rats.We have recently developed an infant rat model with hepatic dysfunction and steatosis induced by overdose of fatfree TPN. 5) After 30 infant (3-week-ol...

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The effect of glutamine-enriched TPN on gut immune cellularity

Cited by 136 publications

References 10 publications

Effects of glutamine supplementation on gut barrier, glutathione content and acute phase response in malnourished rats during inflammatory shock

Effects of glutamine supplementation on gut barrier, glutathione content and acute phase response in malnourished rats during inflammatory shock

Bactericidal Activity Against Coagulase-Negative Staphylococci Is Impaired in Infants Receiving Long-Term Parenteral Nutrition

Soybean Oil Fat Emulsion to Prevent TPN-Induced Liver Damage: Possible Molecular Mechanisms and Clinical Implications

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