Dietary glutamine supplementation prevents mucosal injury and modulates intestinal epithelial restitution following acetic acid induced intestinal injury in rats

Forat Swaid,Christopher Hadjittofi,Igor Sukhotnik,Yulia Pollak,Ibrahim Matter,Alexandra Lavy,Drora Berkowitz

doi:10.1186/1743-7075-10-53

Abstract

Beneficial effects of glutamine (GLN) have been described in many gastrointestinal disorders. The aim of the present study was to evaluate the preventative effect of oral GLN supplementation against acetic acid (AA) induced intestinal injury in a rat. Male Sprague–Dawley rats were divided into four experimental groups: control (CONTR) rats underwent laparotomy, control-glutamine (CONTR-GLN) rats were treated with enteral glutamine given in drinking water (2%) 48 hours before and five days following laparotomy, AA rats underwent laparotomy and injection of AA into an isolated jejunal loop, and acetic acid-glutamine (AA-GLN) rats underwent AA-induced injury and were treated with enteral GLN 48 hours before and 5 days following laparotomy. Intestinal mucosal damage (Park’s injury score), mucosal structural changes, enterocyte proliferation and enterocyte apoptosis were determined five days following intestinal injury. Western blotting was used to determine p-ERK and bax protein levels. AA-induced intestinal injury resulted in a significantly increased intestinal injury score with concomitant inhibition of cell turnover (reduced proliferation and enhanced apoptosis). Treatment with dietary GLN supplementation resulted in a decreased intestinal injury score with concomitant stimulation of cell turnover (enhanced proliferation and reduced apoptosis). In conclusion, pre-treatment with oral GLN prevents mucosal injury and improves intestinal recovery following AA-induced intestinal injury in rats.

Highlights

The identification of factors that prevent mucosal injury during intestinal damage as well as factors that improve intestinal restitution following intestinal injury may reveal new therapeutic strategies for maintaining mucosal integrity of the gastrointestinal (GI) tract, improving outcomes in patients with intestinal inflammation
Extensive studies involving various experimental models have established that GLN is an essential respiratory substrate for cells in the small intestinal mucosa, accounting for over one third of the total CO2 produced in the small intestine [4]
Enteral GLN supplementation (AA-GLN group) resulted in a trend toward increase in final body weight compared to acetic acid (AA) animals; this trend did not achieve statistical significance

Summary

Introduction

The identification of factors that prevent mucosal injury during intestinal damage as well as factors that improve intestinal restitution following intestinal injury may reveal new therapeutic strategies for maintaining mucosal integrity of the gastrointestinal (GI) tract, improving outcomes in patients with intestinal inflammation. Intracolonic administration of acetic acid (AA) has been previously described as a model of experimental colitis [1]. We. GLN is a non-essential amino acid, produced mainly by muscle, and plays an important role in many physiological and biological processes. Recent evidence suggests that GLN is an important nutrient for rapidly dividing cells such as those found in the immune system and gut [3]. Extensive studies involving various experimental models have established that GLN is an essential respiratory substrate for cells in the small intestinal mucosa, accounting for over one third of the total CO2 produced in the small intestine [4]. GLN exerts a positive effect on gut-associated lymphoid tissue and enhances gut barrier function

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