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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 crypt cell proliferation. 5-BrdU incorporation into proliferating jejunal and ileal crypt cells was detected with a goat anti-BrdU antibody. The representative sections (on the right side) demonstrate that cell proliferation decreased following AA-damage compared to control animals. Following administration of oral glutamine, AA-rats demonstrated a marked increase in a number of proliferating cells compared to AA non-treated animals. 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 5: Effect of acetic acid and oral glutamine on crypt cell proliferation. 5-BrdU incorporation into proliferating jejunal and ileal crypt cells was detected with a goat anti-BrdU antibody. The representative sections (on the right side) demonstrate that cell proliferation decreased following AA-damage compared to control animals. Following administration of oral glutamine, AA-rats demonstrated a marked increase in a number of proliferating cells compared to AA non-treated animals. 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: Treatment of control rats with glutamine (CONTR-GLN group) led to a mild increase in cell proliferation rates in ileum (165 ± 3 vs. 141 ± 10 BrdU positive cells/10 crypts, p < 0.05) compared to CONTR rats as well as in a trend toward increase in cell proliferation rates in jejunum; however, this trend was not statistically significant (Figure 5). AA-induced intestinal damage (C-AA rats) resulted in a significant decrease in the enterocyte proliferation index in jejunum (98 ± 10 vs. 136 ± 11 BrdU positive cells/10 crypts, p < 0.05) and ileum (130 ± 12 vs. 141 ± 10 BrdU positive cells/10 crypts, p < 0.05) compared to control animals. Oral glutamine administration (AA-GLN group) induced a significant increase in the proliferation index in ileum (122 ± 4 vs. 98 ± 10 BrdU positive cells/10 crypts, p < 0.05) compared to AA rats. Both AA and AA-GLN rats demonstrated a lower cell proliferation rates compared to CONTR-GLN rats.


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 crypt cell proliferation. 5-BrdU incorporation into proliferating jejunal and ileal crypt cells was detected with a goat anti-BrdU antibody. The representative sections (on the right side) demonstrate that cell proliferation decreased following AA-damage compared to control animals. Following administration of oral glutamine, AA-rats demonstrated a marked increase in a number of proliferating cells compared to AA non-treated animals. 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

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

Figure 5: Effect of acetic acid and oral glutamine on crypt cell proliferation. 5-BrdU incorporation into proliferating jejunal and ileal crypt cells was detected with a goat anti-BrdU antibody. The representative sections (on the right side) demonstrate that cell proliferation decreased following AA-damage compared to control animals. Following administration of oral glutamine, AA-rats demonstrated a marked increase in a number of proliferating cells compared to AA non-treated animals. 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: Treatment of control rats with glutamine (CONTR-GLN group) led to a mild increase in cell proliferation rates in ileum (165 ± 3 vs. 141 ± 10 BrdU positive cells/10 crypts, p < 0.05) compared to CONTR rats as well as in a trend toward increase in cell proliferation rates in jejunum; however, this trend was not statistically significant (Figure 5). AA-induced intestinal damage (C-AA rats) resulted in a significant decrease in the enterocyte proliferation index in jejunum (98 ± 10 vs. 136 ± 11 BrdU positive cells/10 crypts, p < 0.05) and ileum (130 ± 12 vs. 141 ± 10 BrdU positive cells/10 crypts, p < 0.05) compared to control animals. Oral glutamine administration (AA-GLN group) induced a significant increase in the proliferation index in ileum (122 ± 4 vs. 98 ± 10 BrdU positive cells/10 crypts, p < 0.05) compared to AA rats. Both AA and AA-GLN rats demonstrated a lower cell proliferation rates compared to CONTR-GLN rats.

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