ABSTRACT
Autophagy is derived from the Greek auto, meaning self, and phagy, meaning eating, and is a cellular homeostatic mechanism that degrades cytoplasmic components such as long-lived proteins, macromolecular aggregates, and dysfunctional and/or aged organelles, among others, in acidic compartments known as lysosomes. In mammals, three primary forms of autophagy have been described depending on the type of cargo and the mechanism by which the cargo is identified and delivered to the lysosomes: macroautophagy, microautophagy, and chaperone-mediated autophagy. The mechanism by which autophagosomes recognize cargo is via presence of cargo-recognition receptors that label autophagic substrates. In humans, alterations in lipid metabolism is intimately linked with the risk of developing metabolic disorders that are typically observed during obesity and in type 2 diabetes. Cells store fat in cytosolic lipid deposits known as lipid droplets. Lipophagy impacts on lipid metabolism and thereby on whole-body energy balance by degrading lipid stores.
