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2015 ; 43
(4
): 327-33
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Protection by enteral glutamine is mediated by intestinal epithelial cell
peroxisome proliferator-activated receptor-? during intestinal
ischemia/reperfusion
#MMPMID25394240
Peng Z
; Ban K
; Wawrose RA
; Gover AG
; Kozar RA
Shock
2015[Apr]; 43
(4
): 327-33
PMID25394240
show ga
We have demonstrated that enteral glutamine provides protection to the
postischemic gut, and that peroxisome proliferator-activated receptor-? (PPAR?)
plays a role in this protection. Using Cre/lox technology to generate an
intestinal epithelial cell (IEC)-specific PPAR? null mouse model, we now
investigated the contribution of IEC PPAR? to glutamine's local and distant
organ-protective effects. These mice exhibited absence of expression of PPAR? in
the intestine but normal PPAR? expression in other tissues. After 1 h of
intestinal ischemia under isoflurane anesthesia, wild-type and null mice received
enteral glutamine (60 mM) or vehicle followed by 6 h of reperfusion or 7 days in
survival experiments and compared with shams. Small intestine, liver, and lungs
were analyzed for injury and inflammatory parameters. Glutamine provided
significant protection against gut injury and inflammation, with similar
protection in the lung and liver. Changes in systemic tumor necrosis factor-?
reflected those seen in the injured organs. Importantly, mice lacking IEC PPAR?
had worsened injury and inflammation, and glutamine lost its protective effects
in the gut and lung. The survival benefit found in glutamine-treated wild-type
mice was not observed in null mice. Using an IEC-targeted loss-of-function
approach, these studies provide the first in vivo confirmation in native small
intestine and lung that PPAR? is responsible for the protective effects of
enteral glutamine in reducing intestinal and lung injury and inflammation and
improving survival. These data suggest that early enteral glutamine may be a
potential therapeutic modality to reduce shock-induced gut dysfunction and
subsequent distant organ injury.
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