title: Liver autophagy in anorexia nervosa and acute liver injury.
abstract: Autophagy, a lysosomal catabolic pathway for long-lived proteins and damaged organelles, is crucial for cell homeostasis, and survival under stressful conditions. During starvation, autophagy is induced in numerous organisms ranging from yeast to mammals, and promotes survival by supplying nutrients and energy. In the early neonatal period, when transplacental nutrients supply is interrupted, starvation-induced autophagy is crucial for neonates' survival. In adult animals, autophagy provides amino acids and participates in glucose metabolism following starvation. In patients with anorexia nervosa, autophagy appears initially protective, allowing cells to copes with nutrient deprivation. However, when starvation is critically prolonged and when body mass index reaches 13 kg/m(2) or lower, acute liver insufficiency occurs with features of autophagic cell death, which can be observed by electron microscopy analysis of liver biopsy samples. In acetaminophen overdose, a classic cause of severe liver injury, autophagy is induced as a protective mechanism. Pharmacological enhancement of autophagy protects against acetaminophen-induced necrosis. Autophagy is also activated as a rescue mechanism in response to Efavirenz-induced mitochondrial dysfunction. However, Efavirenz overdose blocks autophagy leading to liver cell death. In conclusion, in acute liver injury, autophagy appears as a protective mechanism that can be however blocked or overwhelmed.
authors.affiliation: INSERM, U970, Paris Cardiovascular Research Center (PARCC), 75015 Paris, France ; Université Paris Descartes, Sorbonne Paris Cité, UMR-S970, 75015 Paris, France.
authors.forename: Marouane
authors.initials: M
authors.lastname: Kheloufi
authors.affiliation: INSERM, U970, Paris Cardiovascular Research Center (PARCC), 75015 Paris, France ; Université Paris Descartes, Sorbonne Paris Cité, UMR-S970, 75015 Paris, France.
authors.forename: Chantal M
authors.initials: CM
authors.lastname: Boulanger
authors.affiliation: DHU Unity, Service d'Hépatologie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, 92 110 Clichy, France.
authors.forename: François
authors.initials: F
authors.lastname: Durand
authors.affiliation: INSERM, U970, Paris Cardiovascular Research Center (PARCC), 75015 Paris, France ; Université Paris Descartes, Sorbonne Paris Cité, UMR-S970, 75015 Paris, France ; DHU Unity, Service d'Hépatologie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, 92 110 Clichy, France.
authors.forename: Pierre-Emmanuel
authors.identifier: 0000-0001-9567-1859
authors.initials: PE
authors.lastname: Rautou
mesh_terms: D000818:Animals; D000856:Anorexia Nervosa / Q000473:pathology*; D001343:Autophagy; D056486:Chemical and Drug Induced Liver Injury / Q000473:pathology*; D022781:Hepatocytes / Q000473:pathology*; D006801:Humans; D008099:Liver / Q000473:pathology*; D017114:Liver Failure, Acute; D008954:Models, Biological