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

Swaid F, Sukhotnik I, Matter I, Berkowitz D, Hadjittofi C, Pollak Y, Lavy A - Nutr Metab (Lond) (2013)

Bottom Line: Beneficial effects of glutamine (GLN) have been described in many gastrointestinal disorders.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).

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Surgery, Bnai Zion Medical Center, Haifa, Israel.

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.

No MeSH data available.


Related in: MedlinePlus

Effect of acetic acid and oral glutamine on expression of p-ERK, and bax protein (Western blot) in intestinal mucosal samples. Values are mean ± SEM. CONTR-control; AA- acetic acid; GLN- glutamine. * P < 0.05 vs CONTR rats, † P < 0.05 AA-GLN vs AA rats.
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Figure 7: Effect of acetic acid and oral glutamine on expression of p-ERK, and bax protein (Western blot) in intestinal mucosal samples. Values are mean ± SEM. CONTR-control; AA- acetic acid; GLN- glutamine. * P < 0.05 vs CONTR rats, † P < 0.05 AA-GLN vs AA rats.

Mentions: Decreased cell proliferation rates in AA animals (Groups B and C) were accompanied by decreased levels of p-ERK protein. Interestingly, an increased cell apoptosis was accompanied by decreased bax-protein levels in AA animals (Groups B and C) compared to control animals. Treatment with glutamine (Group C) did not change significantly the levels of p-ERK and Bax protein compared to AA-nontreated animals (Group B) (Figure 7).


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

Swaid F, Sukhotnik I, Matter I, Berkowitz D, Hadjittofi C, Pollak Y, Lavy A - Nutr Metab (Lond) (2013)

Effect of acetic acid and oral glutamine on expression of p-ERK, and bax protein (Western blot) in intestinal mucosal samples. Values are mean ± SEM. CONTR-control; AA- acetic acid; GLN- glutamine. * P < 0.05 vs CONTR rats, † P < 0.05 AA-GLN vs AA rats.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750704&req=5

Figure 7: Effect of acetic acid and oral glutamine on expression of p-ERK, and bax protein (Western blot) in intestinal mucosal samples. Values are mean ± SEM. CONTR-control; AA- acetic acid; GLN- glutamine. * P < 0.05 vs CONTR rats, † P < 0.05 AA-GLN vs AA rats.
Mentions: Decreased cell proliferation rates in AA animals (Groups B and C) were accompanied by decreased levels of p-ERK protein. Interestingly, an increased cell apoptosis was accompanied by decreased bax-protein levels in AA animals (Groups B and C) compared to control animals. Treatment with glutamine (Group C) did not change significantly the levels of p-ERK and Bax protein compared to AA-nontreated animals (Group B) (Figure 7).

Bottom Line: Beneficial effects of glutamine (GLN) have been described in many gastrointestinal disorders.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).

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Surgery, Bnai Zion Medical Center, Haifa, Israel.

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.

No MeSH data available.


Related in: MedlinePlus