Skip to main content
Journal cover image

Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models.

Publication ,  Journal Article
Xue, H; Sufit, AJD; Wischmeyer, PE
Published in: JPEN J Parenter Enteral Nutr
March 2011

BACKGROUND: Pharmacologic doses of glutamine (GLN) can improve clinical outcome following acute illness and injury. Recent studies indicate enhanced heat shock protein (HSP) expression is a key mechanism underlying GLN's protection. However, such a link has not yet been tested in chronic inflammatory states, such as experimental inflammatory bowel disease (IBD). METHODS: Experimental colitis was induced in Sprague-Dawley rats via oral 5% dextran sulfate sodium (DSS) for 7 days. GLN (0.75 g/kg/d) or sham was administered to rats by oral gavage during 7-day DSS treatment. In vitro inflammatory injury was studied using YAMC colonic epithelial cells treated with varying concentrations of GLN and cytokines (tumor necrosis factor-α/interferon-γ). RESULTS: Pharmacologic dose, bolus GLN attenuated DSS-induced colitis in vivo with decreased area under curve for bleeding (8.06 ± 0.87 vs 10.38 ± 0.79, P < .05) and diarrhea (6.97 ± 0.46 vs 8.53 ± 0.39, P < .05). This was associated with enhanced HSP25 and HSP70 in colonic mucosa. In vitro, GLN enhanced cell survival and reduced proapoptotic caspase3 and poly(ADP-ribose) polymerase cleavage postcytokine injury. Cytokine-induced inducible nitric oxide synthase expression and nuclear translocation of nuclear factor-κB p65 subunit were markedly attenuated at GLN concentrations above 0.5 mmol/L. GLN increased cellular HSP25 and HSP70 in a dose-dependent manner. CONCLUSIONS: These data demonstrate the therapeutic potential of GLN as a "pharmacologically acting nutrient" in the setting of experimental IBD. GLN sufficiency is crucial for the colonic epithelium to mount a cell-protective, antiapoptotic, and anti-inflammatory response against inflammatory injury. The enhanced HSP expression observed following GLN treatment may be responsible for this protective effect.

Duke Scholars

Published In

JPEN J Parenter Enteral Nutr

DOI

EISSN

1941-2444

Publication Date

March 2011

Volume

35

Issue

2

Start / End Page

188 / 197

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Poly(ADP-ribose) Polymerases
  • Nutrition & Dietetics
  • Nitric Oxide Synthase Type II
  • NF-kappa B
  • Mice
  • Male
  • Intestinal Mucosa
  • Inflammatory Bowel Diseases
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Xue, H., Sufit, A. J. D., & Wischmeyer, P. E. (2011). Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models. JPEN J Parenter Enteral Nutr, 35(2), 188–197. https://doi.org/10.1177/0148607110381407
Xue, Hongyu, Alexandra J. D. Sufit, and Paul E. Wischmeyer. “Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models.JPEN J Parenter Enteral Nutr 35, no. 2 (March 2011): 188–97. https://doi.org/10.1177/0148607110381407.
Xue H, Sufit AJD, Wischmeyer PE. Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models. JPEN J Parenter Enteral Nutr. 2011 Mar;35(2):188–97.
Xue, Hongyu, et al. “Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models.JPEN J Parenter Enteral Nutr, vol. 35, no. 2, Mar. 2011, pp. 188–97. Pubmed, doi:10.1177/0148607110381407.
Xue H, Sufit AJD, Wischmeyer PE. Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models. JPEN J Parenter Enteral Nutr. 2011 Mar;35(2):188–197.
Journal cover image

Published In

JPEN J Parenter Enteral Nutr

DOI

EISSN

1941-2444

Publication Date

March 2011

Volume

35

Issue

2

Start / End Page

188 / 197

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Poly(ADP-ribose) Polymerases
  • Nutrition & Dietetics
  • Nitric Oxide Synthase Type II
  • NF-kappa B
  • Mice
  • Male
  • Intestinal Mucosa
  • Inflammatory Bowel Diseases