Protein-Energy Malnutrition Alters Thermoregulatory Homeostasis and the Response to Brain Ischemia

Title: Protein-Energy Malnutrition Alters Thermoregulatory Homeostasis and the Response to Brain Ischemia

Volume: 8 Issue: 1

Author(s): Shari E. Smith, Erin J. Prosser-Loose, Frederick Colbourne and Phyllis G. Paterson

Affiliation:

Keywords: Global brain ischemia, protein-energy malnutrition, rat, reactive gliosis, thermoregulation, two-vessel occlusion, Homeostasis

Abstract: Co-existing protein-energy malnutrition (PEM), characterized by deficits in both protein and energy status, impairs functional outcome following global ischemia and has been associated with increased reactive gliosis. Since temperature is a key determinant of brain damage following an ischemic insult, the objective was to investigate whether alterations in post-ischemic temperature regulation contribute to PEM-induced reactive gliosis following ischemia. Male Sprague-Dawley rats (190-280g) were assigned to either control diet (18% protein) or PEM induced by feeding a low protein diet (2% protein) for 7 days prior to either global ischemia or sham surgery. There was a rapid disruption in thermoregulatory function in rats fed the low protein diet as assessed by continuous recording of core temperature with bio-electrical sensor transmitters. Both daily temperature fluctuation and mean temperature increased within the first 24 hours, and these remained significantly elevated throughout the 7 day pre-ischemic period (p < 0.027). In the immediate post-surgical period, PEM decreased body temperature to a greater extent than that in well-nourished controls (p = 0.003). The increase in daily temperature fluctuation caused by PEM persisted throughout the 7 day post-surgical period (p < 0.001), and this interacted with the effects of global ischemia on days 8 (p = 0.018) and 11 (p = 0.021). The astrocytic and microglial responses induced at 7 days after global ischemia were not influenced by PEM, but this preliminary analysis needs to be confirmed with a more reliable global ischemia model. In conclusion, exposure to a low protein diet rapidly impairs the ability to maintain thermoregulatory homeostasis, and the resultant PEM also diminishes the ability to thermoregulate in response to a challenge. Since temperature regulation is a key determinant of brain injury following ischemia, these findings suggest that the pathophysiology of brain injury could be altered in stroke victims with coexisting PEM.

Cite this article as:

E. Smith Shari, J. Prosser-Loose Erin, Colbourne Frederick and G. Paterson Phyllis, Protein-Energy Malnutrition Alters Thermoregulatory Homeostasis and the Response to Brain Ischemia, Current Neurovascular Research 2011; 8 (1) . https://dx.doi.org/10.2174/156720211794520206