The Role of Dietary Supplementation with L-Glutamine in Inflammatory Mediator Release & Intestinal Injury in Hypoxia/Reoxygenation-Induced Experimental Necrotizing Enterocolitis

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The Role of Dietary Supplementation with L-Glutamine in Inflammatory Mediator

Release & Intestinal Injury in Hypoxia/Reoxygenation-induced Experimental

Necrotizing Enterocolitis JoAnn Guest Jun 08, 2005 17:57 PDT

Vol. 47, No. 6, 2003

 

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Original Paper

 

The Role of Dietary Supplementation with L-Glutamine in Inflammatory

Mediator Release and Intestinal Injury in Hypoxia/Reoxygenation-Induced

Experimental Necrotizing Enterocolitis

Mete Akisua, Meral Bakab, Afig Huseyinova, Nilgun Kultursaya

 

Departments of

aPediatrics and

bHistology, Ege University Medical School, Izmir, Turkey

 

 

Address of Corresponding Author

 

Annals of Nutrition & Metabolism 2003;47:262-266 (DOI:

10.1159/000072398)

 

 

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Key Words

 

L-Glutamine

Necrotizing enterocolitis

 

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Abstract

 

Background/Aims: Necrotizing enterocolitis (NEC) is a multifactorial

syndrome in the neonate. Enteral feeding practices are an important

component of gastrointestinal injury in neonatal NEC. In the present

study, we examined the protective effect of oral supplementation with

L-glutamine, an important specific fuel for the enterocytes, against

hypoxia-reoxygenation (H/R)-induced NEC in young mice. Methods: Young

mice were divided into four groups: group 1 mice (untreated) underwent

H/R; group 2 mice were supplemented with L-glutamine in drinking water

(0.5 g/dl) for 3 days, and group 3 mice were supplemented with

L-glutamine (3 g/dl) for 10 days. Group 4 mice served as control.

Hypoxia was induced by placing the young mice in a 100% CO2 chamber for

5 min. After hypoxia, they were reoxygenated for 10 min with 100%

oxygen. We examined the intestinal lesions with light microscopy and

measured intestinal generation of PAF and TNF- in the H/R-induced model

of NEC. Results: In group 3 mice, NEC-induced intestinal tissue damage

was greatly attenuated with necrosis limited partially to the mucosa.

Both intestinal tissue PAF and TNF- concentrations were significantly

higher in the untreated group than in controls (p < 0.001). Group 3 mice

(3 g/dl supplemented) showed a significant decrease in intestinal TNF-

concentration compared with young group 1 and group 2 mice (p < 0.05 and

p < 0.05, respectively). On the other hand, no significant difference

was observed in the intestinal generation of PAF between H/R groups (p >

0.05). Conclusion: The present study suggests that H/R plays an

important role in the pathogenesis of NEC and supports the hypothesis

that especially PAF and TNF- are involved in the pathophysiological

mechanism of H/R-induced NEC. This study also demonstrates that dietary

supplementation with L-glutamine reduces the histologic evidence of

H/R-induced intestinal injury. Based on these findings, beneficial

effects of L-glutamine in this model of NEC are mediated via mechanisms

inhibiting intestinal cytokine release.

 

2003 S. Karger AG, Basel

 

 

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Author Contacts

 

Mete Akisu, MD

Associate Professor in Pediatrics

Department of Pediatrics, Ege University Medical School, Bornova

TR-35100 Izmir (Turkey)

Tel./Fax +90 232 342 6990, E-Mail mak-

 

 

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Article Information

 

Received: December 8, 2002

Accepted: May 8, 2003

Number of Print Pages : 5

Number of Figures : 0, Number of Tables : 2, Number of References : 29

 

 

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