Jpen Parenter Enter
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Jpen Parenter Enter · Sep 2006
Randomized Controlled TrialThe effect of glutamine-enriched enteral nutrition on intestinal permeability in very-low-birth-weight infants: a randomized controlled trial.
Very-low-birth-weight (VLBW) infants are susceptible to glutamine depletion. Glutamine depletion has negative effects on intestinal integrity. The lower infection rate in VLBW infants receiving glutamine-enriched enteral nutrition may originate from improved intestinal integrity, as reflected by decreased intestinal permeability. The aim of our study was to investigate whether glutamine-enriched enteral nutrition in VLBW infants enhances the normal decrease in intestinal permeability, as measured by the sugar absorption test (SAT). ⋯ Glutamine-enriched enteral nutrition does not enhance the postnatal decrease in intestinal permeability in VLBW infants. Any beneficial effect of glutamine may involve other aspects of intestinal integrity; for example, modulation of the intestinal inflammatory response.
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Jpen Parenter Enter · Sep 2006
Glutamine attenuation of cell death and inducible nitric oxide synthase expression following inflammatory cytokine-induced injury is dependent on heat shock factor-1 expression.
Glutamine (GLN) has been shown to improve outcome after experimental and clinical models of critical illness. Enhanced expression of heat shock protein (HSP) has been hypothesized to be responsible for this protection. The heat shock response has been shown to inhibit inducible nitric oxide synthase (iNOS) gene expression and nitric oxide (NO) production. This study tested the hypothesis that GLN-mediated activation of the HSP pathway is responsible for improved survival and attenuation of iNOS expression after an inflammatory cytokine-induced injury. ⋯ This is the first demonstration that GLN-mediated cellular protection after inflammatory cytokine injury is due to HSF-1 expression and cellular capacity to activate an HSP response.
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Jpen Parenter Enter · Sep 2006
Glutamine-mediated attenuation of cellular metabolic dysfunction and cell death after injury is dependent on heat shock factor-1 expression.
Cellular metabolic dysfunction is associated with occurrence of multiple-organ failure after critical illness. Glutamine (GLN) attenuates cellular metabolic dysfunction in critical illness models. The mechanism of this protection is unclear. We previously demonstrated that GLN's benefit in critical illness might be due to enhanced heat shock protein (HSP) expression. We hypothesize that GLN's attenuation of cellular metabolic dysfunction is dependent on presence of heat shock factor-1 (HSF-1). ⋯ GLN treatment attenuated cellular metabolic dysfunction and improved cell membrane recovery only in HSF-1+/+ cells. Cellular injury, as measured by lactate release and cell survival assay, was improved by GLN treatment in HSF-1+/+ cells alone. Thus, GLN's beneficial effect on cellular metabolic dysfunction and cell survival appears to be dependent on HSF-1 expression.
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Jpen Parenter Enter · Sep 2006
Albumin infusion after reperfusion prevents gut ischemia-reperfusion-induced gut-associated lymphoid tissue atrophy.
Our recent study clarified that gut ischemia-reperfusion (I/R) causes gut-associated lymphoid tissue (GALT) mass atrophy, a possible mechanism for increased morbidity of infectious complications after severe surgical insults. Because albumin administration reportedly reduces hemorrhagic shock-induced lung injury, we hypothesized that albumin treatment prevents GALT atrophy due to gut I/R. ⋯ Albumin infusion after a gut ischemic insult may maintain gut immunity by preventing GALT atrophy.
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Jpen Parenter Enter · Sep 2006
Interleukin-7 dose-dependently restores parenteral nutrition-induced gut-associated lymphoid tissue cell loss but does not improve intestinal immunoglobulin a levels.
Without enteral nutrition, the mass and function of gut-associated lymphoid tissue (GALT), a center of systemic mucosal immunity, are reduced. Therefore, new therapeutic methods, designed to preserve mucosal immunity during parenteral nutrition (PN), are needed. Our recent study revealed that exogenous interleukin-7 (IL-7; 1 microg/kg twice a day) restores the GALT cell mass lost during intravenous (IV) PN but does not improve secretory immunoglobulin A (IgA) levels. Herein, we studied the IL-7 dose response to determine the optimal IL-7 dose for recovery of GALT mass and function during IV PN. We hypothesized that a high dose of IL-7 would increase intestinal IgA levels, as well as GALT cell numbers. ⋯ Exogenous IL-7 dose-dependently reverses PN-induced GALT cell loss, with no major changes in small intestinal IgA levels. IL-7 treatment during PN appears to have beneficial effects on gut immunity, but other therapeutic methods are needed to restore secretory IgA levels.