Packaging of Fat: An Evolving Model of Lipid Droplet Assembly and Expansion

Rutgers Center for Lipid Research and Department of Nutritional Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey 08901, USA.
Journal of Biological Chemistry (Impact Factor: 4.57). 11/2011; 287(4):2273-9. DOI: 10.1074/jbc.R111.309088
Source: PubMed


Lipid droplets (LDs) are organelles found in most types of cells in the tissues of vertebrates, invertebrates, and plants,
as well as in bacteria and yeast. They differ from other organelles in binding a unique complement of proteins and lacking
an aqueous core but share aspects of protein trafficking with secretory membrane compartments. In this minireview, we focus
on recent evidence supporting an endoplasmic reticulum origin for LD formation and discuss recent findings regarding LD maturation
and fusion.

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    • "In cells, lipids are safely stored in lipid droplets (LDs)—monolayer membrane-encased organelles which are managed as dynamic repositories of lipids (mainly in the form of cholesterol esters and triglycerides) [1, 2] . LDs also represent locations where key enzymes involved in cholesterol metabolism and fatty acid synthesis regulate the various anabolic and catabolic steps in lipid metabolism [3, 4]. Macrophages are innate immune sentinel cells that also play important roles in the regulation of lipid homeostasis. "
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    ABSTRACT: Nuclear hormone receptors have important roles in the regulation of metabolic and inflammatory pathways. The retinoid-related orphan receptor alpha (Rorα)-deficient staggerer (sg/sg) mice display several phenotypes indicative of aberrant lipid metabolism, including dyslipidemia, and increased susceptibility to atherosclerosis. In this study we demonstrate that macrophages from sg/sg mice have increased ability to accumulate lipids and accordingly exhibit larger lipid droplets (LD). We have previously shown that BMMs from sg/sg mice have significantly decreased expression of cholesterol 25-hydroxylase (Ch25h) mRNA, the enzyme that produces the oxysterol, 25-hydroxycholesterol (25HC), and now confirm this at the protein level. 25HC functions as an inverse agonist for RORα. siRNA knockdown of Ch25h in macrophages up-regulates Vldlr mRNA expression and causes increased accumulation of LDs. Treatment with physiological concentrations of 25HC in sg/sg macrophages restored lipid accumulation back to normal levels. Thus, 25HC and RORα signify a new pathway involved in the regulation of lipid homeostasis in macrophages, potentially via increased uptake of lipid which is suggested by mRNA expression changes in Vldlr and other related genes.
    Full-text · Article · Jan 2016 · PLoS ONE
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    • "In the late phase of adipocyte differentiation, PLIN2 expression gradually declines and is replaced by PLIN1 in mature adipocytes [101]. PLIN2 primarily localizes to the surface of LDs as do PLIN1, whereas PLIN3 is stable in the cytoplasm and relocates to nascent LDs upon increased TAG synthesis [102]. "
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    ABSTRACT: Cytosolic lipid droplets are dynamic lipid-storage organelles that play a crucial role as reservoirs of metabolic energy and membrane precursors. These organelles are present in virtually all cell types, from unicellular to pluricellular organisms. Despite similar structural organization, lipid droplets are heterogeneous in morphology, distribution and composition. The protein repertoire associated to lipid droplet controls the organelle dynamics. Distinct structural lipid droplet proteins are associated to specific lipolytic pathways. The role of these structural lipid droplet-associated proteins in the control of lipid droplet degradation and lipid store mobilization is discussed. The control of the strictly-regulated lipolysis in lipid-storing tissues is compared between mammals and plants. Differences in the cellular regulation of lipolysis between lipid-storing tissues and other cell types are also discussed. Copyright © 2015. Published by Elsevier B.V.
    Full-text · Article · Jul 2015 · Biochimie
    • "Each neutral lipid core of a LD has a coat consisting of a phospholipid monolayer, with phosphatidylcholine providing the quantitatively major component. Other polar lipids contribute, such as cholesterol and nonesterified fatty acids (Robenek et al., 2011; Brasaemle and Wolins, 2012). The amphipathic monolayer prevents multilocular LDs from coalescing into very large LDs and provides docking stations for proteins. "

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