Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis. | Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis.: Lipid metabolism in amyotrophic lateral sclerosis mice
Fergani, Anissa | Oudart, Hugues | Gonzalez de Aguilar, Jose-Luis | Fricker, Bastien | René, Frédérique | Hocquette, Jean-François | Meininger, Vincent | Dupuis, Luc | Loeffler, Jean-Philippe | Laboratoire de signalisation moléculaire et neurodégénerescence ; Université Louis Pasteur - Strasbourg I-IFR37-Institut National de la Santé et de la Recherche Médicale (INSERM) | Département Ecologie, Physiologie et Ethologie (DEPE-IPHC) ; Institut Pluridisciplinaire Hubert Curien (IPHC) ; Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS)-Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS) | Unité de Recherches sur les Herbivores (URH) ; Institut National de la Recherche Agronomique (INRA) | CHU Pitié-Salpêtrière [AP-HP] ; Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
International audience
Показать больше [+] Меньше [-]Английский. Amyotrophic lateral sclerosis (ALS) is the most common adult motor neuron disease, causing motor neuron degeneration, muscle atrophy, paralysis, and death. Despite this degenerative process, a stable hypermetabolic state has been observed in a large subset of patients. Mice expressing a mutant form of Cu/Zn-superoxide dismutase (mSOD1 mice) constitute an animal model of ALS that, like patients, exhibits unexpectedly increased energy expenditure. Counterbalancing for this increase with a high-fat diet extends lifespan and prevents motor neuron loss. Here, we investigated whether lipid metabolism is defective in this animal model. Hepatic lipid metabolism was roughly normal, whereas gastrointestinal absorption of lipids as well as peripheral clearance of triglyceride-rich lipoproteins were markedly increased, leading to decreased postprandial lipidemia. This defect was corrected by the high-fat regimen that typically induces neuroprotection in these animals. Together, our findings show that energy metabolism in mSOD1 mice shifts toward an increase in the peripheral use of lipids. This metabolic shift probably accounts for the protective effect of dietary lipids in this model.
Показать больше [+] Меньше [-]Ключевые слова АГРОВОК
Библиографическая информация
Эту запись предоставил Institut national de la recherche agronomique