Retinyl ester hydrolases and their roles in vitamin A homeostasis

Abstract

In mammals, dietary vitamin A intake is essential for the maintenance of adequate retinoid (vitamin A and metabolites) supply of tissues and organs. Retinoids are taken up from animal or plant sources and subsequently stored in form of hydrophobic, biologically inactive retinyl esters (REs). Accessibility of these REs in the intestine, the circulation, and their mobilization from intracellular lipid droplets depends on the hydrolytic action of RE hydrolases (REHs). In particular, the mobilization of hepatic RE stores requires REHs to maintain steady plasma retinol levels thereby assuring constant vitamin A supply in times of food deprivation or inadequate vitamin A intake. In this review, we focus on the roles of extracellular and intracellular REHs in vitamin A metabolism. Furthermore, we will discuss the tissue-specific function of REHs and highlight major gaps in the understanding of RE catabolism. This article is part of a Special Issue entitled Retinoid and Lipid Metabolism.

Fig. 1

Retinoid fluxes and RE hydrolyzing enzymes. Depiction of major retinoid fluxes between tissues and organs, which are involved in the uptake, transport, storage, and utilization of retinoids. Identified REHs of respective organs, tissues, and cell types are given in parenthesis. REH activities of unidentified proteins are indicated as “?”. Percent of total bodies RE stores are given for major storage tissues and cell-types. Abbreviations: CEL, carboxylester lipase; Es2/3/4/10/22, esterase2/3/4/10/22; GS2, gene sequence 2; HSL, hormone-sensitive lipase; LPL, lipoprotein lipase; PLRP2, pancreatic lipase related protein 2; PTL, pancreatic triglyceride lipase; RPE65, retinal pigment epithelium 65.