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dc.contributor.author
Lucero, Diego Martín
dc.contributor.author
Miksztowicz, Verónica
dc.contributor.author
Macri, Vanesa
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López, Gustavo H.
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Friedman, Silvia
dc.contributor.author
Berg, Gabriela
dc.contributor.author
Zago, Valeria
dc.contributor.author
Schreier, Laura Ester
dc.date.available
2020-11-05T16:40:07Z
dc.date.issued
2015-07
dc.identifier.citation
Lucero, Diego Martín; Miksztowicz, Verónica; Macri, Vanesa; López, Gustavo H.; Friedman, Silvia; et al.; Overproduction of altered VLDL in an insulin-resistance rat model: Influence of SREBP-1c and PPAR-α; Elsevier Doyma Sl; Clínica e Investigación en Arteriosclerosis; 27; 4; 7-2015; 167-174
dc.identifier.issn
0214-9168
dc.identifier.uri
http://hdl.handle.net/11336/117689
dc.description.abstract
Background: In insulin-resistance, VLDL presents alterations that increase its atherogenic potential. The mechanism by which insulin-resistance promotes the production of altered VLDL is still not completely understood. The aim of this study was to evaluate the relationship between the expression of sterol regulatory element binding protein 1c (SREBP-1c) and of peroxisome proliferator-activated receptor-α (PPAR-α), with the features of composition and size of VLDL in an insulin-resistance rat model induced by a sucrose rich diet (SRD). Methods: The study was conducted on 12 male Wistar rats (180 g) receiving SRD (12 weeks) and 12 controls. Lipid profile, free fatty acids, glucose, and insulin were measured. Lipid content in liver and visceral fat were assessed. Isolated VLDL (d< 1.006. g/ml) was characterized by its chemical composition and size by HPLC. The respective hepatic expression of SREBP-1c and PPAR-α was determined (Western blot). Results: As expected, SRD had elevated triglycerides (TG), free fatty acids and insulin levels, and decreased HDL-cholesterol (p< 0.05), together with augmented hepatic and visceral fat (p< 0.05). SRD showed higher VLDL total mass - with increased TG content - and predominance of large VLDL (p< 0.05). SRD showed an increase in SREBP-1c (precursor and mature forms) and decreased PPAR-α expression (p<0.045). SREBP-1c forms were positively associated with VLDL total mass ( p< 0.04), VLDL-TG% ( p< 0.019), and large VLDL% (p< 0.002). On the other hand, PPAR-α correlated negatively with VLDL total mass ( p= 0.05), VLDL-TG% ( p= 0.005), and large VLDL% ( p= 0.002). Conclusions: Insulin-resistance, by coordinated activation of SREBP-1c and reduction of PPAR-α, could promote the secretion of larger and TG over-enriched VLDL particles, with greater atherogenic capacity.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Doyma Sl
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
INSULIN-RESISTANCE
dc.subject
LARGE VERY LOW DENSITY LIPOPROTEIN
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PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-Α
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STEROL REGULATORY ELEMENT BINDING PROTEIN 1C
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SUCROSE RICH DIET
dc.subject.classification
Otras Ciencias de la Salud
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Ciencias de la Salud
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Overproduction of altered VLDL in an insulin-resistance rat model: Influence of SREBP-1c and PPAR-α
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-09-08T14:00:56Z
dc.identifier.eissn
1578-1879
dc.journal.volume
27
dc.journal.number
4
dc.journal.pagination
167-174
dc.journal.pais
España
dc.journal.ciudad
Madrid
dc.description.fil
Fil: Lucero, Diego Martín. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
dc.description.fil
Fil: Miksztowicz, Verónica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
dc.description.fil
Fil: Macri, Vanesa. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Bioquímica General y Bucal; Argentina
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Fil: López, Gustavo H.. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Cátedra Bioanalitica Ii; Argentina
dc.description.fil
Fil: Friedman, Silvia. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Bioquímica General y Bucal; Argentina
dc.description.fil
Fil: Berg, Gabriela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
dc.description.fil
Fil: Zago, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
dc.description.fil
Fil: Schreier, Laura Ester. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
dc.journal.title
Clínica e Investigación en Arteriosclerosis
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0214916814001703
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1016/j.arteri.2014.11.002
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