Abstract
For mammals, vitamin A (retinol and metabolites) is an essential micronutrient that is required for the maintenance of life. Mammals cannot synthesize vitamin A but have to obtain it from their diet. Resorbed dietary vitamin A is stored in large quantities in the form of retinyl esters (REs) in cytosolic lipid droplets of cells to ensure a constant supply of the body. The largest quantities of REs are stored in the liver, comprising around 80% of the body’s total vitamin A content. These hepatic vitamin A stores are known to be mobilized under times of insufficient dietary vitamin A intake but also under pathological conditions such as chronic alcohol consumption and different forms of liver diseases. The mobilization of REs requires the activity of RE hydrolases. It is astounding that despite their physiological significance little is known about their identities as well as about factors or stimuli which lead to their activation and consequently to the mobilization of hepatic RE stores. In this review, we focus on the recent advances for the understanding of hepatic RE hydrolases and discuss pathological conditions which lead to the mobilization of hepatic RE stores.
Highlights
The turnover of vitamin A involves two major metabolites, retinol and the esterified form of retinol, retinyl ester (RE)
We focus on the recent advances for the understanding of hepatic RE hydrolases and discuss pathological conditions which lead to the mobilization of hepatic RE stores
Over the last few decades, the generation of transgenic and knock-out mouse models as well as the development of techniques for the overexpression/silencing of genes in cultured cells has significantly advanced the understanding of protein function
Summary
The turnover of vitamin A (retinol and metabolites) involves two major metabolites, retinol and the esterified form of retinol, retinyl ester (RE). Retinol is esterified to REs and packed into chylomicrons for secretion Another example is the hepatic utilization of vitamin A [3]: in liver, hepatocytes take up RE-containing chylomicron remnants via the endocytic pathway. Retinol is esterified to REs and stored in cytosolic lipid droplets (LDs) of hepatocytes and even more so in hepatic stellate cells (HSCs). Hepatic RE stores are mobilized under times of insufficient vitamin A intake [9,10], and upon certain types of liver diseases [11,12,13] Despite this essential role of hepatic RE hydrolases, the identity of enzymes responsible for the hydrolysis of RE stores is largely unknown. These cells are known to perform most of the liver’s functions in carbohydrate, fat, bile acid, and protein metabolism [15]
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