Glutamine stimulates amino acid transport during ischemia-reperfusion in human intestinal epithelial cells

Wasa, Masafumi; Wang, H.S.; Shimizu, Yasuhisa; Fukuzawa, Moe

doi:10.1016/j.jss.2003.08.184

Cited by 11 publications

(13 citation statements)

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“…[48][49][50] In models of ischemia-reperfusion, it was established that iNOS gene expression decreased in subjects fed a glutamine-supplemented diet. [51] It is also known that glutamine acts as an important step in GSH synthesis. On the other hand, NF-κB activation is closely associated with intracellular redox balance and the GSH/GSSG ratio.…”

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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“…As Gln transporters are decreased in several pathological conditions such as in short-bowel syndrome [9,22], interventions are needed to increase their long-term activity by de-novo synthesis of transporters. However, under certain conditions, such as in response to feeding after fasting, salivation (saliva contains EGF), and ischemia reperfusion injury with swelling, short-term increases in Gln transporters are crucial [2,4,37]. We have investigated the mechanisms involved in short-term upregulation of Gln transporters by EGF in an intestinal cell line.…”

Section: Discussionmentioning

confidence: 99%

“…In intestinal cell models, Gln prevents increased permeability after fasting [2] or treatment with acetaldehyde [3] and stimulates amino acid transport after ischemia-reperfusion injury [4].…”

Section: Introductionmentioning

confidence: 99%

In Human Entrocytes, GLN Transport and ASCT2 Surface Expression Induced by Short-Term EGF are MAPK, PI3K, and Rho-Dependent

2007

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Glutamine, a key nutrient for the enterocyte, is transported among other proteins by ASCT2. Epidermal growth factor (EGF) augments intestinal adaptation. We hypothesized that short-term treatment of human enterocytes with EGF enhances glutamine transport by increasing membranal ASCT2. To elucidate EGF-induced mechanisms, monolayers of C2(BBe)1 w/wo siRho transfection were treated w/wo EGF and w/wo tyrphostin AG1478 (AG1478), wortmanin, or PD98059. Total and system-specific (3)H-glutamine transports were determined w/wo 5 mmol/l amino acid inhibitors. Total and membranal ASCT2 proteins were measured by Westerns. EGF doubled glutamine transport by increasing B(0)/ASCT2 and B(0,+) activities. Despite the doubling of membranal ASCT2 protein with EGF treatment, total ASCT2 did not change. The increases in B(0)/ASCT2 activity and ASCT2 protein were eliminated by AG1478, PD98059, wortmanin, and siRho, while transport by B(0,+) was inhibited only by PD98059 and siRho. Thus, differential pathways are involved in EGF-induced increase in B(0)/ASCT2 glutamine transport and membranal ASCT2 compared to those involved in B(0,+) activity.

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“…19 The levels of N-acetylglutamine and N-a-acetylcitrulline, which are associated with nervous system functions, were elevated in the samples collected at 2 h, 5 h, 8 h and 12 h and reduced at 24 h, 36 h and 48 h, suggesting that the nervous system is disturbed in THBSS. 20,21 The levels of iduronic acid and homocysteine sulnic acid, which can affect coagulation function, were altered, demonstrating the dysfunction of coagulation during THBSS progression.…”

Section: Metabonomics Analysismentioning

confidence: 99%

Holistic and dynamic metabolic alterations of traditional Chinese medicine syndrome in a toxic heat and blood stasis syndrome rat model

Shen

et al. 2017

RSC Adv.

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Metabonomic analysis has been widely used in the study of traditional Chinese medicine (TCM) syndromes.In this paper, dynamic changes of the metabolic network during the evolution of a syndrome based on the toxic heat and blood stasis syndrome (THBSS) rat model have been elucidated for the first time. It was found that the metabolic trajectories could characterize three stages during THBSS evolution: the metabolic disturbance at 2-5 h, 8-12 h and 24-48 h could reflect the status of the excessive heat and little blood stasis stage, the coexistence of heat and blood stasis stage and the blood stasis stage respectively. The obtained dynamic metabolic network revealed the mechanism of THBSS progression: the inhibition of nicotinate and nicotinamide metabolism may lead to the activation of SIRT1 producing an inflammatory response, which then results in the disorder of energy metabolism and amino acid metabolism, and eventually the blood stasis appears. Nine involved metabolic pathways were found, among which the nicotinate and nicotinamide metabolism and histidine metabolism closely related to the occurrence of the inflammatory response in the early stage and blood stasis in the later stage of THBSS respectively.The former one, which is not reported in other blood stasis syndromes, might be the characteristic pathway of THBSS. This study firstly reveals the essence of THBSS progression, which is conducive to the diagnosis and pharmacotherapeutics of THBSS and related diseases, and also provides a new way to study TCM syndrome evolution.

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Glutamine stimulates amino acid transport during ischemia-reperfusion in human intestinal epithelial cells

Cited by 11 publications

References 0 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

In Human Entrocytes, GLN Transport and ASCT2 Surface Expression Induced by Short-Term EGF are MAPK, PI3K, and Rho-Dependent

Holistic and dynamic metabolic alterations of traditional Chinese medicine syndrome in a toxic heat and blood stasis syndrome rat model

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