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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M700017-JLR200 on April 16, 2007

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Journal of Lipid Research, Vol. 48, 1571-1580, July 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosisboxs

Anissa Fergani*,{dagger}, Hugues Oudart§, Jose-Luis Gonzalez De Aguilar*,{dagger}, Bastien Fricker*,{dagger}, Frédérique René*,{dagger}, Jean-François Hocquette**, Vincent Meininger{dagger}{dagger}, Luc Dupuis1,*,{dagger} and Jean-Philippe Loeffler*,{dagger}

* Institut National de la Santé et de la Recherche Médicale, U692, Laboratoire de Signalisations Moléculaires et Neurodégénérescence, Strasbourg, F-67085 France
{dagger} Université Louis Pasteur, Faculté de Médecine, Unité Mixte de Recherche S692, Strasbourg, F-67085 France
§ Centre d'Ecologie et Physiologie Energétiques, Unité Propre de Recherche 9010, Centre National de la Recherche Scientifique, 67087 Strasbourg Cedex, France
** Equipe Croissance et Metabolismes du Muscle, Unite de Recherches sur les Herbivores, Institut National de la Recherche Agronomique, Centre de Clermont-Ferrand/Theix, 63122 St Genes-Champanelle, France
{dagger}{dagger} Fédération des Maladies du Système Nerveux, Centre Référent Maladie Rare Sclerose Lateral Amyotrophique, Hôpital de la Pitié-Salpêtrière, 75651 Paris, France

boxs The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of a table.

Published, JLR Papers in Press, April 16, 2007.

1 To whom correspondence should be addressed. e-mail: ldupuis{at}neurochem.u-strasbg.fr

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.

Supplementary key words plasma lipoproteins • neurodegeneration • motor neuron • low density lipoprotein • high density lipoprotein • liver metabolism • intestinal absorption • skeletal muscle


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