Abstract
Autophagy is a lysosomal pathway by which intracellular organelles and proteins are degraded to supply the cell with energy and to maintain cellular homeostasis. Recently, lipid droplets (LDs) have been identified as a substrate for macroautophagy. In addition to the classic pathway of lipid metabolism by cytosolic lipases, LDs are sequestered in autophagosomes that fuse with lysosomes for the breakdown of LD components by lysosomal enzymes. The ability of autophagy to respond to changes in nutrient supply allows the cell to alter LD metabolism to meet the cell's energy demands. Pathophysiological changes in autophagic function can alter cellular lipid metabolism and promote disease states. Autophagy therefore represents a new cellular target for abnormalities in lipid metabolism and accumulation.