Once formed, lipid droplets can fuse with each other or transfer material by a slow coalescence event. The growth of LDs and the incorporation of FAs into TAG is a fast event, typically taking just a few minutes. ĭepending on cell type, nutritional status and developmental state the LD pool can vary in droplet number, size and localization within short time scales. The TAG secreted as CM and VLDL mainly derives from TAG stored in cytosolic LDs. In the absence of loaded lipids apoB cannot be secreted and is rapidly degraded. While VLDL and CM contain apoE, apoC and apoB, LDL harbors exclusively apoB. In contrast to other apolipoproteins, apoB is not exchangeable between lipoproteins and resides in the plasma in a lipid-associated form only. The major neutral lipid, triacylglycerol (TAG), is secreted from the liver and intestine in apolipoproteinB (apoB) containing lipoproteins (CM and VLDL). They are classified into chylomicrons (CM), very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins based on their apolipoprotein component and their density, which is determined by the lipid composition. These lipoproteins are soluble complexes of proteins (apolipoproteins) and lipids that are transported in the circulation of vertebrates and insects and that are synthesized in the liver and intestine. Extracellularly, the bulk of lipids is transported in lipoproteins.
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Furthermore, lipids are exchanged between different tissues. Within cells they can move within membranes and between different cellular compartments. Lipids are in a constant flux and are continuously converted into each other. Therefore, it is crucial to understand how the storage of lipids is regulated under normal conditions. The first step is usually the excess storage of lipids within different body tissues resulting in the development of obesity. Many metabolic disorders like diabetes and cardiovascular diseases are associated with defects in lipid metabolism and derive from additive defects in different pathways, often described as metabolic syndrome that can gradually progress into more severe diseases. Different proteins are associated with the LDs, including several enzymes of lipid metabolism. LDs consist of a core of neutral lipids that is surrounded by a monolayer of phospholipids, mainly phosphatidylcholine. The cellular location of storage of neutral lipid is the lipid droplet (LD). Lipids are important components of cells, with a function in cellular structure, regulation, signaling and as energy source, in particular neutral lipids. Differences in lipid droplet size may account for differences in lipid dynamics and be relevant to understand lipid overload diseases.
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ConclusionĪctivity of the Kennedy pathway regulates the balance between phospholipids and neutral lipids, while the Lands cycle regulates lipid droplet size by regulating surface availability and influencing surface to volume ratio.
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Furthermore we demonstrate that modulation of the LD pool by LPCAT1 influences the release of lipoprotein from liver cells. We show that function of LPCAT1 and 2 is conserved in Drosophila melanogaster by the ortholog CG32699.
DENSITOMETRY WAS DONE WITH IMAGEJ SOFTWARE PC
Here, we show that knock-down of both enzymes leads to an increase in LD size without changes in the total amount of neutral lipids, while interference with the de-novo Kennedy pathway PC biosynthesis is associated with changes in triacylglyceride synthesis. We have recently shown that two Lands cycle PC synthesizing enyzmes, LPCAT1 and LPCAT2 can localize to the LD surface. These dynamics require a fast adaptation of LD surface. LDs are very dynamic and can rapidly change in size upon lipid uptake or release. They consist of a core of neutral lipids surrounded by a monolayer of phospholipids, predominantly phosphatidylcholine (PC). Lipids are stored within cells in lipid droplets (LDs).