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dc.contributor.authorMocciaro, Gabriele
dc.contributor.authorD'Amore, Simona
dc.contributor.authorJenkins, Benjamin
dc.contributor.authorKay, Richard
dc.contributor.authorMurgia, Antonio
dc.contributor.authorHerrera-Marcos, Luis Vicente
dc.contributor.authorNeun, Stefanie
dc.contributor.authorSowton, Alice
dc.contributor.authorHall, Zoe
dc.contributor.authorPalma-Duran, Susana Alejandra
dc.contributor.authorPalasciano, Giuseppe
dc.contributor.authorReimann, Frank
dc.contributor.authorMurray, Andrew
dc.contributor.authorSuppressa, Patrizia
dc.contributor.authorSabbà, Carlo
dc.contributor.authorMoschetta, Antonio
dc.contributor.authorKoulman, Albert
dc.contributor.authorGriffin, Julian L
dc.contributor.authorVacca, Michele
dc.description.abstractThe metabolic syndrome (MetS) is a cluster of cardiovascular risk factors characterised by central obesity, atherogenic dyslipidaemia, and changes in the circulating lipidome; the underlying mechanisms that lead to this lipid remodelling have only been partially elucidated. This study used an integrated "omics" approach (untargeted whole serum lipidomics, targeted proteomics, and lipoprotein lipidomics) to study lipoprotein remodelling and HDL composition in subjects with central obesity diagnosed with MetS (vs. controls). Compared with healthy subjects, MetS patients showed higher free fatty acids, diglycerides, phosphatidylcholines, and triglycerides, particularly those enriched in products of de novo lipogenesis. On the other hand, the "lysophosphatidylcholines to phosphatidylcholines" and "cholesteryl ester to free cholesterol" ratios were reduced, pointing to a lower activity of lecithin cholesterol acyltransferase (LCAT) in MetS; LCAT activity (directly measured and predicted by lipidomic ratios) was positively correlated with high-density lipoprotein cholesterol (HDL-C) and negatively correlated with body mass index (BMI) and insulin resistance. Moreover, many phosphatidylcholines and sphingomyelins were significantly lower in the HDL of MetS patients and strongly correlated with BMI and clinical metabolic parameters. These results suggest that MetS is associated with an impairment of phospholipid metabolism in HDL, partially led by LCAT, and associated with obesity and underlying insulin resistance. This study proposes a candidate strategy to use integrated "omics" approaches to gain mechanistic insights into lipoprotein remodelling, thus deepening the knowledge regarding the molecular basis of the association between MetS and atherosclerosis.
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.titleLipidomic Approaches to Study HDL Metabolism in Patients with Central Obesity Diagnosed with Metabolic Syndrome.
dc.publisher.departmentDept of Physiology, Development and Neuroscience
prism.publicationNameInt J Mol Sci
dc.contributor.orcidMocciaro, Gabriele [0000-0001-5392-0909]
dc.contributor.orcidD'Amore, Simona [0000-0002-5432-8808]
dc.contributor.orcidJenkins, Benjamin [0000-0003-0038-9709]
dc.contributor.orcidHerrera-Marcos, Luis Vicente [0000-0002-4665-9674]
dc.contributor.orcidNeun, Stefanie [0000-0002-2469-6984]
dc.contributor.orcidSowton, Alice [0000-0002-3718-7783]
dc.contributor.orcidMurray, Andrew [0000-0002-0929-9315]
dc.contributor.orcidMoschetta, Antonio [0000-0003-2123-6074]
dc.contributor.orcidKoulman, Albert [0000-0001-9998-051X]
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MC_UU_12012/3)
pubs.funder-project-idMedical Research Council (MC_UU_12012/5)
pubs.funder-project-idMedical Research Council (MR/M009041/1)
pubs.funder-project-idBritish Heart Foundation (FS/17/61/33473D)
pubs.funder-project-idNational Institute for Health Research (IS-BRC-1215-20014)
pubs.licence-display-nameApollo Repository Deposit Licence Agreement

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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International