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dc.contributor.author
Mazzucco, María Belén
dc.contributor.author
Fornes, Daiana
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Capobianco, Evangelina Lorena
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Jawerbaum, Alicia Sandra
dc.date.available
2017-03-10T20:46:25Z
dc.date.issued
2016-01
dc.identifier.citation
Mazzucco, María Belén; Fornes, Daiana; Capobianco, Evangelina Lorena; Jawerbaum, Alicia Sandra; Maternal saturated fat-rich diet promotes leptin resistance in fetal liver lipid catabolism and programs lipid homeostasis impairments in the liver of rat offspring; Elsevier Inc; Journal Of Nutritional Biochemistry; 27; 1-2016; 61-69
dc.identifier.issn
0955-2863
dc.identifier.uri
http://hdl.handle.net/11336/13729
dc.description.abstract
We aimed to analyze if an overload of saturated fat in maternal diet induced lipid metabolic impairments in livers from rat fetuses that persist in the offspring and to identify potential mechanisms involving fetal leptin resistance. Female rats were fed either a diet enriched in 25% of saturated fat (SFD rats) or a regular diet (controls). Fetuses of 21 days of gestation and offspring of 21 and 140 days of age were obtained and plasma and liver were kept for further analysis. Livers from a group of control and SFD fetuses were cultured in the presence or absence of leptin. Leptin or vehicle was administered to control fetuses during the last days of gestation and, on day 21, fetal livers and plasma were obtained. Lipid levels were assessed by thin-layer chromatography and mRNA gene expression of CPT1, ACO and PPARα by RT-PCR. Liver lipid levels were increased and CPT1 and ACO were down-regulated in fetuses and offspring from SFD rats compared to controls. After the culture with leptin, control fetal livers showed increased ACO and CPT1 expression and decreased lipid levels, while fetal livers from SFD rats showed no changes. Fetal administration of leptin induced a decrease in ACO and no changes in CPT1 expression. In summary, our results suggest that a saturated fat overload in maternal diet induces fetal leptin resistance in liver lipid catabolism, which might be contributing to liver lipid alterations that are sustained in the offspring.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Inc
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subject
Leptin
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Liver Catabolism
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Saturated Fat Rich Diet
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Offspring
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Fetus
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Otras Ciencias Médicas
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Otras Ciencias Médicas
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Maternal saturated fat-rich diet promotes leptin resistance in fetal liver lipid catabolism and programs lipid homeostasis impairments in the liver of rat offspring
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2017-03-09T15:07:10Z
dc.journal.volume
27
dc.journal.pagination
61-69
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Mazzucco, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
dc.description.fil
Fil: Fornes, Daiana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
dc.description.fil
Fil: Capobianco, Evangelina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
dc.description.fil
Fil: Jawerbaum, Alicia Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
dc.journal.title
Journal Of Nutritional Biochemistry
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S095528631500220X
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.jnutbio.2015.08.019


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