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dc.contributor.author
Lucero, Diego Martín
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dc.contributor.author
Svidirov, Denis
dc.contributor.author
Freeman, Lita
dc.contributor.author
López, Graciela I.
dc.contributor.author
Fassio, Eduardo
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dc.contributor.author
Remaley, Alan T.
dc.contributor.author
Schreier, Laura Ester
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dc.date.available
2020-11-05T16:38:42Z
dc.date.issued
2015-09
dc.identifier.citation
Lucero, Diego Martín; Svidirov, Denis; Freeman, Lita; López, Graciela I.; Fassio, Eduardo; et al.; Increased cholesterol efflux capacity in metabolic syndrome: Relation with qualitative alterations in HDL and LCAT; Elsevier Ireland; Atherosclerosis; 242; 1; 9-2015; 236-242
dc.identifier.issn
0021-9150
dc.identifier.uri
http://hdl.handle.net/11336/117684
dc.description.abstract
Background: Metabolic syndrome (MetS) is associated with changes in HDL levels, composition and sub-fraction profile. Whether these alterations affect HDL anti-atherogenic function, specifically measured as its capacity to perform cholesterol efflux, is not yet clearly known. Objective: To evaluate the relation between serum cholesterol efflux capacity and the changes in HDL composition and sub-fraction profile in MetS. Methods: In 35 non-treated MetS patients and 15 healthy controls, HDL mediated cholesterol efflux was measured as the ability of apoB-depleted serum to accept cholesterol from cholesterol-loaded BHK cells expressing either ABCA1 or ABCG1. Additionally we determined: lipid profile, HDL sub-fractions (NMR) and LCAT mass (ELISA). Isolated HDL (δ:1.063-1.210 g/mL) was chemically characterized. Pre-β1-HDL was determined by 2D-electrophoresis in a sub-group of MetS and controls (n = 6 each). Results: Surprisingly, MetS patients presented higher ABCA1 mediated cholesterol efflux (10.4 ± 1.8 vs. 8.7 ± 0.3%; p = 0.0001), without differences in ABCG1 efflux. In MetS, HDL showed reduction in particle size and number (p < 0.02) and lower large/small HDL ratio (p = 0.05), as well as triglyceride enrichment (p = 0.0001). Pre-β1-HDL was increased in MetS (p = 0.048) and correlated with ABCA1-cholesterol efflux (r = 0.64; p = 0.042). LCAT mass showed a tendency to reduction in MetS (p = 0.08), and inversely correlated with ABCA1-cholesterol efflux (r = -0.51; p = 0.001), independently of obesity and insulin-resistance (β = -0.40, p = 0.034). Conclusion: This is the first description of ABCA1 mediated cholesterol efflux in MetS. Regardless the reduced HDL-cholesterol, in vitro cholesterol efflux capacity by ABCA1 was enhanced, linked to increased pre-β1-HDL and slightly reduced in LCAT mass that would probably reflect a delay in reverse cholesterol transport occurring in MetS.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Ireland
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
CHOLESTEROL EFFLUX CAPACITY
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HDL
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LCAT
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METABOLIC SYNDROME
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PRE-Β1-HDL
dc.subject.classification
Otras Ciencias de la Salud
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dc.subject.classification
Ciencias de la Salud
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Increased cholesterol efflux capacity in metabolic syndrome: Relation with qualitative alterations in HDL and LCAT
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-09-08T13:58:19Z
dc.journal.volume
242
dc.journal.number
1
dc.journal.pagination
236-242
dc.journal.pais
Irlanda
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dc.description.fil
Fil: Lucero, Diego Martín. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
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Fil: Svidirov, Denis. National Institutes of Health; Estados Unidos
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Fil: Freeman, Lita. National Institutes of Health; Estados Unidos
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Fil: López, Graciela I.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina
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Fil: Fassio, Eduardo. Hospital Nacional Profesor Alejandro Posadas; Argentina
dc.description.fil
Fil: Remaley, Alan T.. National Institutes of Health; Estados Unidos
dc.description.fil
Fil: Schreier, Laura Ester. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina
dc.journal.title
Atherosclerosis
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0021915015300393
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1016/j.atherosclerosis.2015.07.019
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