Evidence for impairment of hepatic energy homeostasis in head-injured rat
| Autor: | Luc Cynober, Séverine Gupta, Valérie C. Besson, Catherine Marchand-Leroux, Béatrice Morio, Christine Charrueau, Jean-Claude Chaumeil, Christophe Moinard |
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| Přispěvatelé: | Processus d’adaptation métaboliques et nouvelles stratégies nutritionnelles (EA 2498), Université Paris Descartes - Paris 5 (UPD5), Unité de Nutrition Humaine (UNH), Institut National de la Recherche Agronomique (INRA)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP) |
| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Male
medicine.medical_specialty LIVER Traumatic brain injury [SDV]Life Sciences [q-bio] Metabolic adaptation Mitochondria Liver Anorexia Mitochondrion GLYCOGEN Energy requirement Energy homeostasis Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Adenosine Triphosphate MITOCHONDRIA Internal medicine medicine Animals Craniocerebral Trauma Homeostasis Nutritional Physiological Phenomena HEAD TRAUMA 030304 developmental biology Gastrostomy 0303 health sciences Glycogen business.industry medicine.disease Rats nervous system diseases ATP Parenteral nutrition Endocrinology chemistry nervous system Neurology (clinical) medicine.symptom business Energy Metabolism Glycolysis 030217 neurology & neurosurgery |
| Zdroj: | Journal of Neurotrauma Journal of Neurotrauma, Mary Ann Liebert, 2008, 25 (2), pp.124-129. ⟨10.1089/neu.2007.0391⟩ |
| ISSN: | 0897-7151 |
| DOI: | 10.1089/neu.2007.0391⟩ |
| Popis: | International audience; 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. |
| Databáze: | OpenAIRE |
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