Document Detail


Fatty acids from very low-density lipoprotein lipolysis products induce lipid droplet accumulation in human monocytes.
MedLine Citation:
PMID:  20208007     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
One mechanism by which monocytes become activated postprandially is by exposure to triglyceride-rich lipoproteins such as very low-density lipoproteins (VLDL). VLDL are hydrolyzed by lipoprotein lipase at the blood-endothelial cell interface, releasing free fatty acids. In this study, we examined postprandial monocyte activation in more detail, and found that lipolysis products generated from postprandial VLDL induce the formation of lipid-filled droplets within cultured THP-1 monocytes, characterized by coherent antistokes Raman spectroscopy. Organelle-specific stains revealed an association of lipid droplets with the endoplasmic reticulum, confirmed by electron microscopy. Lipid droplet formation was reduced when lipoprotein lipase-released fatty acids were bound by BSA, which also reduced cellular inflammation. Furthermore, saturated fatty acids induced more lipid droplet formation in monocytes compared with mono- and polyunsaturated fatty acids. Monocytes treated with postprandial VLDL lipolysis products contained lipid droplets with more intense saturated Raman spectroscopic signals than monocytes treated with fasting VLDL lipolysis products. In addition, we found that human monocytes isolated during the peak postprandial period contain more lipid droplets compared with those from the fasting state, signifying that their development is not limited to cultured cells but also occurs in vivo. In summary, circulating free fatty acids can mediate lipid droplet formation in monocytes and potentially be used as a biomarker to assess an individual's risk of developing atherosclerotic cardiovascular disease.
Authors:
Laura J den Hartigh; Jaime E Connolly-Rohrbach; Samantha Fore; Thomas R Huser; John C Rutledge
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-03-05
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  184     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-22     Completed Date:  2010-04-27     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3927-36     Citation Subset:  AIM; IM    
Affiliation:
Division of Endocrinology, Department of Internal Medicine, University of California, Davis, Davis, CA 95616, USA.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Cells, Cultured
Endoplasmic Reticulum / metabolism,  ultrastructure
Enzyme-Linked Immunosorbent Assay
Fatty Acids / metabolism*
Female
Humans
Lipid Metabolism / physiology*
Lipolysis / physiology*
Lipoproteins, VLDL / metabolism*
Male
Microscopy, Electron, Scanning
Middle Aged
Monocytes / metabolism*,  ultrastructure
Postprandial Period / physiology
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha / biosynthesis
Young Adult
Grant Support
ID/Acronym/Agency:
HL055667/HL/NHLBI NIH HHS; R01 AG039094/AG/NIA NIH HHS; R01 HL055667/HL/NHLBI NIH HHS; R01 HL055667-08/HL/NHLBI NIH HHS; UL1 RR024146/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Lipoproteins, VLDL; 0/Tumor Necrosis Factor-alpha
Comments/Corrections

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