Glutamine and the gastrointestinal tract

Ziegler, Thomas R.; Bazargan, Niloofar; Leader, Lorraine M.; Martindale, Robert G.

doi:10.1097/00075197-200009000-00005

Cited by 83 publications

(59 citation statements)

References 67 publications

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“…If the effect of the blood-intestine barrier is considered in sepsis, the importance of prevention of oxidative damage and bacterial translocation can be recognized. [24,25] The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model Cilt -Vol. 17 Sayı -No.…”

Section: Discussionmentioning

confidence: 99%

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

Tıhan

Erbil²,

Seven³

et al. 2011

Ulus Travma Acil Cerrahi Derg

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AMAÇBu çalışmada, antioksidan özelliği bilinen glutaminin kullanımının iskemi-reperfüzyon sonrası oluşabilecek oksidasyon hasarı üzerindeki etkilerini araştırmayı amaçladık. GEREÇ VE YÖNTEMÇalışma grubu Wistar Albino sıçanlarla oluşturuldu. Grup 1, abdominal kompartman grubuydu. Anestezi altındaki sı-çanların karnına basınç uygulandı. Gaz boşaltıldıktan 3 gün sonra sıçanlar sakrifiye edildi, karaciğer, bağırsak ve akciğer doku parçalarında oksidatif hasar parametresi olarak malonildialdehit (MDA) ve glutatyon (GSH) seviyeleri ile enflamatuvar parametre olarak miyeloperoksidaz (MPO) aktivitesi ölçüldü. Alınan kan örneklerinde serum alaninaminoasit transferaz (ALT) ve aspartat-aminoasit transferaz (AST) seviyeleri ölçüldü. Grup 2, abdominal kompartman ve glutamin uygulanan gruptu. Sıçanlara 1 hafta boyunca yüksek doz glutamin mide gavajı yolu ile verildi. Gavaj işlemi sonrası ilk gruptaki batın içi basınç uygulaması yapıldı, 3 gün daha glutamin verilen sıçanlar sakrifiye edildi, Grup 1'deki işlemlerin aynısı yapıldı. Grup 3 glutamin grubuydu. Grup 4 sham kontrol grubuydu. BULGULARAbdominal kompartman yaratılan sıçanlarda MDA düzeyi ve MPO aktivitesi kontrol grubuna göre anlamlı oranda artmıştı. Glutamin ile MDA düzeyi ve MPO aktivitesi azaldı, GSH seviyesi arttı. SONUÇOksidatif hasar parametrelerine bakıldığında, glutaminin, reperfüzyon hasarını azaltıcı etkisinin antienflamatuvar ve antioksidan etkilerine bağlı olduğu düşünülmüştür.

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Section: Discussionmentioning

confidence: 99%

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

Tıhan

Erbil²,

Seven³

et al. 2011

Ulus Travma Acil Cerrahi Derg

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“…Glutamine is used as a major fuel and nucleotide substrate for rapidly dividing cells such as intestinal mucosal cells and the gut-associated immunocytes [33][34][35][36][37] . Glutamine can prevent atrophy of the intestinal epithelial cells through HSP 70 generation [38] and improve the intestinal immune barrier [39][40][41] . A meta-analysis by Novak F et al [42] revealed that glutamine could reduce the infectious morbidity (RR 0.84, 95% CI: 0.68-1.03) and mortality (RR 0.76, 95% CI: 0.56-0.98) in critical illness.…”

Section: Discussionmentioning

confidence: 99%

Impact of alanyl-glutamine dipeptide on severe acute pancreatitis in early stage

Xue

Deng²,

Xia³

et al. 2008

WJG

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INTRODUCTIONAcute pancreatitis (AP) contributes to thousands of annual hospital admissions, of which severe acute pancreatitis (SAP) accounts for 10%-20% [1][2][3] . Despite considerable improvement in the treatment, the mortality of SAP still ranges between 10%-15% [2][3][4][5] . The course of SAP tends to be prolonged and the patients usually are hypermetabolic and high protein catabolic due to systemic inflammatory response syndrome (SIRS) induced by acute local inflammatory process and subsequent vital-organ dysfunction [6] . Thus, if nutritive support is not appropriately administrated to match rapidly increased demand in the treatment of SAP, the patients consequently come down with metabolic disorder and nutrition deficiency, which is considered to increase mortality due to impaired immune function, increased risk of infections and intractable vital-organ failure.In recent years, research showed a conditional deficiency of glutamine would be an independent predictive factor for a poor outcome and its correction improved survival by restoring cellular protective mechanisms, improving immune function and resistance of the gut barrier to hypoperfusion, metabolic stress and subsequent bacterial translocation, and decreasing the risk of infection in critical illness [7][8][9][10] . Since free glutamine is instable in solution, intravenous administration is limited [7] . Alanyl-glutamine METHODS:Eighty patients with SAP were randomized and received 100 mL/d of 20% AGD intravenously for 10 d starting either on the day of (early treatment group) or 5 d after (late treatment group) admission. Groups had similar demographics, underlying diseases, Ranson score, Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score, and Balthazar 's computed tomography (CT) score at the beginning of the study and underwent similar other medical and nutritional management. RESULTS:The duration of acute respiratory distress syndrome (2.7 ± 3.3 d vs 12.7 ± 21.0 d, P < 0.01), renal failure (1.3 ± 0.5 d vs 5.3 ± 7.3 d, P < 0.01), acute hepatitis (3.2 ± 2.3 d vs 7.0 ± 7.1 d, P < 0.01), shock (1.7 ± 0.4 d vs 4.8 ± 3.1 d, P < 0.05), encephalopathy (2.3 ± 1.9 d vs 9.5 ± 11.0 d, P < 0.01) and enteroparalysis (2.2 ± 1.4 d vs 3.5 ± 2.2 d, P < 0.01) and hospital stay (28.8 ± 9.4 d vs 45.2 ± 27.1 d, P < 0.01) were shorter in the early treatment group than in the late treatment group. The 15-d APACHE Ⅱ score was lower in the early treatment group than in the late treatment group (5.0 ± 2.4 vs 8.6 ± 3.6, P < 0.01). The infection rate (7.9% vs 26.3%, P < 0.05), operation rate (13.2% vs 34.2%, P < 0.05) and mortality (5.3% vs 21.1%, P < 0.05) in the early treatment group were lower than in the late treatment group.Xue P et al . Impact of AGD on SAP 475 www.wjgnet.com dipeptide (AGD), however, can be taken via vein and hydrolyzed into alanine and glutamine in circulation as a substitute [7] . Presently AGD supplement in parenteral nutrition is a worth-trying approach and an evidence-based recommendation in the management of SAP [11] , but ...

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“…Gln is a preferred respiratory fuel and can contribute to cellular energy supply in intestinal epithelial cells (28,30,42). Ala was unable to substitute for Gln in stimulating Caco-2 cell BrdU incorporation.…”

Section: Discussionmentioning

confidence: 99%

“…A growing number of investigations indicate that supplementation with the amino acid glutamine (Gln) stimulates growth, repair, and barrier function of the gut epithelia (30,42). Gln is a major respiratory fuel for intestinal mucosal cells in vivo and is required for optimal cell proliferation in vitro (27,38,41).…”

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confidence: 99%

Glutamine and KGF each regulate extracellular thiol/disulfide redox and enhance proliferation in Caco-2 cells

Jonas

Gu²,

Nkabyo³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Glutamine (Gln) and keratinocyte growth factor (KGF) each stimulate intestinal epithelial cell growth, but regulatory mechanisms are not well understood. We determined whether Gln and KGF alter intra-and extracellular thiol/disulfide redox pools in Caco-2 cells cultured in oxidizing or reducing cell medium and whether such redox variations are a determinant of proliferative responses to these agents. Cells were cultured over a physiological range of oxidizing to reducing extracellular thiol/disulfide redox (E h) conditions, obtained by varying cysteine (Cys) and cystine (CySS) concentrations in cell medium. Cell proliferation was determined by 5-bromo-2-deoxyuridine (BrdU) incorporation. Gln (10 mmol/l) or KGF (10 g/l) did not alter BrdU incorporation at reducing E h (Ϫ131 to Ϫ150 mV), but significantly increased incorporation at more oxidizing E h (Gln at 0 to Ϫ109 mV; KGF at Ϫ46 to Ϫ80 mV). Cellular glutathione/glutathione disulfide (GSH/GSSG) E h was unaffected by Gln, KGF, or variations in extracellular Cys/CySS E h. Control cells largely maintained extracellular E h at initial values after 24 h (Ϫ36 to Ϫ136 mV). However, extracellular E h shifted toward a narrow physiological range with Gln and KGF treatment (Gln Ϫ56 to Ϫ88 mV and KGF Ϫ76 to Ϫ92 mV, respectively; P Ͻ 0.05 vs. control). The results indicate that thiol/disulfide redox state in the extracellular milieu is an important determinant of Caco-2 cell proliferation induced by Gln and KGF, that this control is independent of intracellular GSH redox status, and that both Gln and KGF enhance the capability of Caco-2 cells to modulate extremes of extracellular redox.

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Glutamine and the gastrointestinal tract

Cited by 83 publications

References 67 publications

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

Impact of alanyl-glutamine dipeptide on severe acute pancreatitis in early stage

Glutamine and KGF each regulate extracellular thiol/disulfide redox and enhance proliferation in Caco-2 cells

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