Literature DB >> 31938290

Glutamine protects intestinal mucosa and promotes its transport after burn injury in rats.

Yan Shi1, Zi-En Wang1,2, Wei Wu1, Dan Wu1, Chao Wang1, Xi Peng1.   

Abstract

Glutamine is an important energy source for intestinal epithelial cells (IEC); however, it is still controversial whether glutaminecan be fully utilized under pathological conditions. In this study, we investigated the changes in glutamine transport after burns and assessed the effects of exogenous glutamine administration. Finally, the potential underlying mechanisms were explored. Experimental rats were randomly divided into three groups: control group (C); burn group (B); burn+glutamine group (B+G). Rats in groups B+G and B received intragastric administration of isodose glutamine or alanine, respectively. At days 1, 3 and 5 after burns, the structure of intestinal mucosa and brush-border membrane vesicles (BBMV) were observed. The glutamine transport capacity of IEC and BBMV was detected. The synthesis of glutamine transporter ASCT2 and B0AT1 was determined. Moreover, the intestinal mucosal blood flow (IMBF), diamine oxidase activity, and the glutamine and ATP content were measured. The results showed that burn injury caused structural damage to IECs and BBMV, and significantly impaired the ability for glutamine transportation. Moreover, the mRNA and protein expressions of ASCT2 and B0AT1 as well as the glutamine and ATP content were markedly decreased. Compared with group B, most of these indicators in group B+G showed significant improvement, and approached normal levels. We conclude that glutamine administration can relieve intestinal damage, improve IMBF, promote energy synthesis and alleviate endoplasmic reticulum stress after burn injury. Finally, the synthesis and modification of ASCT2 and B0AT1 are promoted, which ultimately enhances intestinal glutamine transport. IJCEP
Copyright © 2018.

Entities:  

Keywords:  BBMV; Glutamine; burn; glutamine transport; intestine

Year:  2018        PMID: 31938290      PMCID: PMC6958174     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


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