Lipid droplet proteins and hepatic lipid metabolism

Lipid droplet (LD) is an intracellular organelle that stores neutral lipids including triglycerides, cholesterol ester, and retinyl ester. LD is not a passive depot of excess lipids but is a metabolically active organelle that interacts with endoplasmic reticulum, mitochondria and other cellular compartment to regulate fate of intracellular lipids. As the increase in size and number of LD is a key feature of hepatosteatosis, information regarding LD biogenesis and mobilization is highly relevant to hepatic lipid metabolism. Lipid droplet proteins represented by perilipins (PLIN) reside on the surface of LD and contribute to stabilization and degradation of LD through their interactions with neutral lipids and lipid metabolic enzymes. For example PLIN1, a prototypical PLIN enriched in adipocytes, prevents lipolysis at un-stimulated state but supports robust increase in lipolysis upon cAMP dependent protein kinase (PKA) activation by regulating access of lipases to LD. The presence of 4 PLINs (PLIN1, PLIN2, PLIN3, and PLIN5) with distinct characteristics is reported in normal liver and that affected by hepatosteatosis. Here, we discuss the current knowledge regarding expression and functions of each PLIN in the liver at physiological and pathological status.