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. Author manuscript; available in PMC: 2011 Jun 15.
Published in final edited form as: J Surg Res. 2009 Jul 17;161(2):288–294. doi: 10.1016/j.jss.2009.06.024

Fig. 1. Overview of the proposed mechanisms for differential modulation of gut function by enteral glutamine and arginine in the hypoperfused gut.

Fig. 1

Following gut ischemia/reperfusion (IR), the proinflammatory transcription factor, AP-1, is increased, as is the downstream, proinflammatory enzyme iNOS. Both are associated with gut inflammation, mucosal injury, and dysfunction. When the enteral nutrient, arginine, is added to the hypoperfused gut, iNOS expression and AP-1 DNA-binding activity are further increased. Arginine is a known precursor to iNOS, but the mechanism by which arginine increases AP-1 is unknown. There is a recently described, NO-mediated protein kinase G pathway that may explain the increase in AP-1 by arginine. PPARγ is believed to inhibit the proinflammatory pathway at the level of AP-1, protecting the hypoperfused gut. Glutamine increases PPARγ DNA-binding activity and may be a novel PPARγ agonist. When PPAR γ is activated, it heterodimerizes with the retinoic acid receptor (RXR) and then binds to the peroxisome proliferator response element (PPRE), resulting in target gene expression.