title: 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.
authors.affiliation: Laboratoire de Biologie de la Nutrition EA 2498, Faculté de Pharmacie, Université Paris Descartes, Paris, France.
authors.forename: Christophe
authors.initials: C
authors.lastname: Moinard
authors.forename: Severine
authors.initials: S
authors.lastname: Gupta
authors.forename: Valerie
authors.initials: V
authors.lastname: Besson
authors.forename: Beatrice
authors.initials: B
authors.lastname: Morio
authors.forename: Catherine
authors.initials: C
authors.lastname: Marchand-Leroux
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Chaumeil
authors.forename: Luc
authors.initials: L
authors.lastname: Cynober
authors.forename: Christine
authors.initials: C
authors.lastname: Charrueau
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000855:Anorexia / Q000378:metabolism; D006259:Craniocerebral Trauma / Q000378:metabolism* / Q000503:physiopathology*; D004734:Energy Metabolism / Q000502:physiology*; D005774:Gastrostomy; D006003:Glycogen / Q000378:metabolism; D006019:Glycolysis / Q000502:physiology; D006706:Homeostasis / Q000502:physiology*; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008930:Mitochondria, Liver / Q000201:enzymology; D009747:Nutritional Physiological Phenomena; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000255:Adenosine Triphosphate; D006003:Glycogen