[Effects of glutamine on the intestinal failure in rats model of acute necrotizing pancreatitis].
OBJECTIVE
To determine the effects of glutamine (Gln) on the intestinal failure in rats with acute necrotizing pancreatitis (ANP) and its possible mechanisms.


METHODS
Fifty-four Sprague-Dawley rats were randomly divided into 3 groups: sham operation (SO, n = 18), ANP (n = 18), and ANP treated with Gln (ANP + Gln, n = 18). ANP model was induced by injection of 5% sodium taurocholate solution into bilo-pancreatic duct. The therapy was continuously given with amino acid solution by a mini-pump via a central intravenous line. In addition, the ANP + Gin group was received 3% Gln dipeptide solution (equal to 2% Gln) with a dosage of 0.5g x kg(-1) x d(-1). These groups were isocaloric and isonitrogenous. Bacterial cultures from pancreas, mesenteric lymph node (MLN), liver, spleen and ascites were done at 24, 48, 72 h after operation. Endotoxin level in portal vein was determined. Pathologic changes of intestinal mucosa were also studied. Apoptosis of intestinal mucosa was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. Expressions of insulin-like growth factor 1 (IGF-1), Gln synthetase (GSase) and glutaminase (Glnase) mRNA were assayed by reverse transcription polymerase chain reaction (RT-PCR).


RESULTS
At 24, 48, 72h, the positive rate of bacterial culture and the endotoxin concentration were increased significantly in ANP group compared to the SO group (P < 0.05), while Gln could decrease them significantly. Pathologic study showed that the height of mucosal villous in ANP group was lower than that in SO group, indicating the intestinal mucosa became more atrophy. However, the height of mucosal villous in ANP + Gln group was no significantly difference compared to that in SO group, indicated Gln could preserve the mucosa well. Apoptotic index was increased in ANP group and decreased in Gln treated rats. Expressions of IGF-1, GSase, Glnase mRNA were down-regulated in ANP group, but were up-regulated in ANP + Gln group.


CONCLUSIONS
The intestinal barrier function was impaired in ANP. Gln could protect intestinal barrier function. This action was probably related to its enhancement of IGF-1, GSase and Glnase mRNA expressions and its inhibition of intestinal mucosal apoptosis.
Wang
X
X
Department of Gastroenterology, Shanghai First People's Hospital, Shanghai 200080, China.
Wu
K
K
Wang
B
B
Xu
X
X
Xu
M
M
Gong
Z
Z
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015536:Down-Regulation; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000378:metabolism; D005972:Glutaminase / Q000235:genetics / Q000378:metabolism; D005973:Glutamine / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D007413:Intestinal Mucosa / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D019283:Pancreatitis, Acute Necrotizing / Q000473:pathology / Q000503:physiopathology*; D012333:RNA, Messenger / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation
D012333:RNA, Messenger; D005973:Glutamine; D007334:Insulin-Like Growth Factor I; D005972:Glutaminase; D005974:Glutamate-Ammonia Ligase