Protein-energy malnutrition impairs functional outcome in global ischemia

• Published in: Experimental neurology 2005-12, Vol.196 (2), p.308-315
• Main Authors: Bobyn, P. Joan, Corbett, Dale, Saucier, Deborah M., Noyan-Ashraf, M. Hossein, Juurlink, Bernhard H.J., Paterson, Phyllis G.
• Format: Article
• Language: English
• Subjects: Animals; Behavior, Animal; Cell Survival; Cerebral ischemia, global; Disease Models, Animal; Exploratory Behavior - physiology; Gerbillinae; Gerbils; Glutathione - metabolism; Glutathione Reductase - metabolism; Hippocampus - pathology; Ischemia - complications; Ischemia - metabolism; Ischemia - pathology; Male; Neurons - pathology; Nutrition; Outcome Assessment (Health Care); Oxidative stress; Protein-energy malnutrition; Protein-Energy Malnutrition - complications; Protein-Energy Malnutrition - metabolism; Protein-Energy Malnutrition - pathology; Statistics as Topic; Time Factors
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/j.expneurol.2005.08.006

We investigated whether protein-energy malnutrition (PEM) exacerbates brain injury in global ischemia. It was hypothesized that PEM would increase secondary brain damage by worsening ischemia-induced depletion of glutathione (GSH) and increasing oxidative stress. Adult male gerbils were fed an adequate protein (12.5%; C) or low protein (2%; PEM) diet for 4 weeks and subjected to 5 min of bilateral carotid artery occlusion (Ischemia) or sham surgery (Sham). At 12 h post-ischemia, GSH and markers of oxidative stress were measured in hippocampus and neocortex. The remaining gerbils were tested in the open field on days 3, 7, and 10, with viable hippocampal CA1 neurons assessed on day 10. Although the habituation of C-Ischemia gerbils in the open field was normal by day 7, PEM-Ischemia gerbils failed to habituate even by day 10 and spent greater time in the outer zone ( P