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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\u2019 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\u2009kg\/m\n                    <jats:sup>2<\/jats:sup>\n                    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.\n                  <\/jats:p>","DOI":"10.1155\/2014\/701064","type":"journal-article","created":{"date-parts":[[2014,8,27]],"date-time":"2014-08-27T17:03:45Z","timestamp":1409159025000},"page":"1-10","source":"Crossref","is-referenced-by-count":66,"title":["Liver Autophagy in Anorexia Nervosa and Acute Liver Injury"],"prefix":"10.1155","volume":"2014","author":[{"given":"Marouane","family":"Kheloufi","sequence":"first","affiliation":[{"name":"INSERM, U970, Paris Cardiovascular Research Center (PARCC), 75015 Paris, France"},{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris Cit\u00e9, UMR-S970, 75015 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chantal M.","family":"Boulanger","sequence":"additional","affiliation":[{"name":"INSERM, U970, Paris Cardiovascular Research Center (PARCC), 75015 Paris, 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