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International Journal of Cell Biology
Volume 2012, Article ID 282041, 12 pages
http://dx.doi.org/10.1155/2012/282041
Review Article

Lipophagy: Connecting Autophagy and Lipid Metabolism

Rajat Singh1,2,3 and Ana Maria Cuervo1,3,4,5

1Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA
2Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
3Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
4Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
5Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY 10461, USA

Received 5 December 2011; Accepted 17 January 2012

Academic Editor: Anne Simonsen

Copyright © 2012 Rajat Singh and Ana Maria Cuervo. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lipid droplets (LDs), initially considered “inert” lipid deposits, have gained during the last decade the classification of cytosolic organelles due to their defined composition and the multiplicity of specific cellular functions in which they are involved. The classification of LD as organelles brings along the need for their regulated turnover and recent findings support the direct contribution of autophagy to this turnover through a process now described as lipophagy. This paper focuses on the characteristics of this new type of selective autophagy and the cellular consequences of the mobilization of intracellular lipids through this process. Lipophagy impacts the cellular energetic balance directly, through lipid breakdown and, indirectly, by regulating food intake. Defective lipophagy has been already linked to important metabolic disorders such as fatty liver, obesity and atherosclerosis, and the age-dependent decrease in autophagy could underline the basis for the metabolic syndrome of aging.