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Evidence for impairment of hepatic energy homeostasis in head-injured rat.

Abstract
Traumatic brain injury (TBI) is known to induce a metabolic adaptation characterized by a nitrogen transfer from the periphery to the liver. However, the consequences of TBI on liver energy status are poorly documented. We evaluated the consequences of TBI on liver energy homeostasis in rats. In a first set of experiments, rats were randomized into two groups: a TBI group traumatized by fluid percussion, and an ad libitum fed group (AL) of healthy rats. The rats were sacrificed at 2, 3, or 4 days (D2, D3, and D4, respectively to determine the kinetic of hepatic energy changes). Since TBI leads to a profound anorexia, in a second set of experiments TBI rats received enteral nutrition (TBI-EN group) for 4 days to specifically assess the role of anorexia in the hepatic disturbances. TBI led to a decrease in hepatic glycogen (D2: TBI 3.9 +/- 1.9 vs. AL 18.9 +/- 2.6 mg/g, p < 0.05) and ATP (D2: TBI 540 +/- 57 vs. AL 850 +/- 44 nmol/g, p < 0.05) contents. These effects were not linked to anorexia, since they were observed when rats were fed using continuous enteral nutrition. Interestingly, there was no adaptation of the mitochondrial oxidative capacity to compensate for the increase in energy requirements (cytochrome C oxidase activity: AL, 82 +/- 5; TBI, 82 +/- 4; and TBI-EN, 87 +/- 3 micromol/min/g, NS). These findings demonstrate that TBI is responsible for an impairment of liver energy homeostasis. Moreover, these alterations are related neither to anorexia nor to decreased mitochondrial oxidative capacity.
AuthorsChristophe Moinard, Severine Gupta, Valerie Besson, Beatrice Morio, Catherine Marchand-Leroux, Jean-Claude Chaumeil, Luc Cynober, Christine Charrueau
JournalJournal of neurotrauma (J Neurotrauma) Vol. 25 Issue 2 Pg. 124-9 (Feb 2008) ISSN: 0897-7151 [Print] United States
PMID18260795 (Publication Type: Journal Article)
Chemical References
  • Adenosine Triphosphate
  • Glycogen
Topics
  • Adenosine Triphosphate (metabolism)
  • Animals
  • Anorexia (metabolism)
  • Craniocerebral Trauma (metabolism, physiopathology)
  • Energy Metabolism (physiology)
  • Gastrostomy
  • Glycogen (metabolism)
  • Glycolysis (physiology)
  • Homeostasis (physiology)
  • Liver (enzymology, metabolism)
  • Male
  • Mitochondria, Liver (enzymology)
  • Nutritional Physiological Phenomena
  • Rats
  • Rats, Sprague-Dawley

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