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Maternal saturated-fat-rich diet promotes leptin resistance in fetal liver lipid catabolism and programs lipid homeostasis impairments in the liver of rat offspring.
Mazzucco, María Belén; Fornes, Daiana; Capobianco, Evangelina; Higa, Romina; Jawerbaum, Alicia; White, Verónica.
Afiliação
  • Mazzucco MB; Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, School of Medicine, University of Buenos Aires, 1053 Buenos Aires, Argentina.
  • Fornes D; Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, School of Medicine, University of Buenos Aires, 1053 Buenos Aires, Argentina.
  • Capobianco E; Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, School of Medicine, University of Buenos Aires, 1053 Buenos Aires, Argentina.
  • Higa R; Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, School of Medicine, University of Buenos Aires, 1053 Buenos Aires, Argentina.
  • Jawerbaum A; Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, School of Medicine, University of Buenos Aires, 1053 Buenos Aires, Argentina.
  • White V; Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, School of Medicine, University of Buenos Aires, 1053 Buenos Aires, Argentina. Electronic address: vernica73@gmail.com.
J Nutr Biochem ; 27: 61-9, 2016 Jan.
Article em En | MEDLINE | ID: mdl-26383539
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 21days of gestation and offspring of 21 and 140days 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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Gorduras na Dieta / Leptina / Fígado Limite: Animals Idioma: En Revista: J Nutr Biochem Assunto da revista: BIOQUIMICA / CIENCIAS DA NUTRICAO Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Argentina País de publicação: Estados Unidos
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Gorduras na Dieta / Leptina / Fígado Limite: Animals Idioma: En Revista: J Nutr Biochem Assunto da revista: BIOQUIMICA / CIENCIAS DA NUTRICAO Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Argentina País de publicação: Estados Unidos