Articles producció científica> Enginyeria Electrònica, Elèctrica i Automàtica

Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long-term hepatic steatosis and insulin resistance.

  • Dades identificatives

    Identificador: imarina:3854708
    Handle: https://hdl.handle.net/20.500.11797/imarina3854708
    Autors:
    Ramon-Krauel, MartaPentinat, ThaisBloks, Vincent WCebria, JudithRibo, SilviaPerez-Wienese, RickyVila, MariaPalacios-Marin, IvonneFernandez-Perez, AntonioVallejo, MarioTellez, NoeliaAngel Rodriguez, MiguelYanes, OscarLerin, CarlesDiaz, RubenPlosch, TorstenTietge, Uwe J FJimenez-Chillaron, Josep C
    Resum:
    Postnatal overfeeding increases the risk of chronic diseases later in life, including obesity, insulin resistance, hepatic steatosis, and type 2 diabetes. Epigenetic mechanisms might underlie the long-lasting effects associated with early nutrition. Here we aimed to explore the molecular pathways involved in early development of insulin resistance and hepatic steatosis, and we examined the potential contribution of DNA methylation and histone modifications to long-term programming of metabolic disease. We used a well-characterized mouse model of neonatal overfeeding and early adiposity by litter size reduction. Neonatal overfeeding led to hepatic insulin resistance very early in life that persisted throughout adulthood despite normalizing food intake. Up-regulation of monoacylglycerol O-acyltransferase ( Mogat) 1 conceivably mediates hepatic steatosis and insulin resistance through increasing intracellular diacylglycerol content. Early and sustained deregulation of Mogat1 was associated with a combination of histone modifications that might favor Mogat1 expression. In sum, postnatal overfeeding causes extremely rapid derangements of hepatic insulin sensitivity that remain relatively stable until adulthood. Epigenetic mechanisms, particularly histone modifications, could contribute to such long-lasting effects. Our data suggest that targeting hepatic monoacylglycerol acyltransferase activity during early life might provide a novel strategy to improve hepatic insulin sensitivity and prevent late-onset insulin resistance and fatty liver disease.-Ramon-Krauel, M., Pentinat, T., Bloks, V. W., Cebrià, J., Ribo, S., Pérez-Wienese, R., Vilà, M., Palacios-Marin, I., Fernández-Pérez, A., Vallejo, M., Téllez, N., Rodríguez, M. À., Yanes, O., Lerin, C., Díaz, R., Plosch, T., Tietge

  • Altres:

    Autor segons l'article: Ramon-Krauel, Marta; Pentinat, Thais; Bloks, Vincent W; Cebria, Judith; Ribo, Silvia; Perez-Wienese, Ricky; Vila, Maria; Palacios-Marin, Ivonne; Fernandez-Perez, Antonio; Vallejo, Mario; Tellez, Noelia; Angel Rodriguez, Miguel; Yanes, Oscar; Lerin, Carles; Diaz, Ruben; Plosch, Torsten; Tietge, Uwe J F; Jimenez-Chillaron, Josep C
    Departament: Enginyeria Electrònica, Elèctrica i Automàtica
    Autor/s de la URV: Rodríguez Merayo, María Araceli / Yanes Torrado, Óscar
    Paraules clau: Weight-gain O-acyltransferase 1 Nutritional epigenetics Neonatal overfeeding Mouse model Monoacylglycerol acyltransferase Mice Lipid-accumulation In-utero High-fat diet Glucose Expression Childhood obesity
    Resum: Postnatal overfeeding increases the risk of chronic diseases later in life, including obesity, insulin resistance, hepatic steatosis, and type 2 diabetes. Epigenetic mechanisms might underlie the long-lasting effects associated with early nutrition. Here we aimed to explore the molecular pathways involved in early development of insulin resistance and hepatic steatosis, and we examined the potential contribution of DNA methylation and histone modifications to long-term programming of metabolic disease. We used a well-characterized mouse model of neonatal overfeeding and early adiposity by litter size reduction. Neonatal overfeeding led to hepatic insulin resistance very early in life that persisted throughout adulthood despite normalizing food intake. Up-regulation of monoacylglycerol O-acyltransferase ( Mogat) 1 conceivably mediates hepatic steatosis and insulin resistance through increasing intracellular diacylglycerol content. Early and sustained deregulation of Mogat1 was associated with a combination of histone modifications that might favor Mogat1 expression. In sum, postnatal overfeeding causes extremely rapid derangements of hepatic insulin sensitivity that remain relatively stable until adulthood. Epigenetic mechanisms, particularly histone modifications, could contribute to such long-lasting effects. Our data suggest that targeting hepatic monoacylglycerol acyltransferase activity during early life might provide a novel strategy to improve hepatic insulin sensitivity and prevent late-onset insulin resistance and fatty liver disease.-Ramon-Krauel, M., Pentinat, T., Bloks, V. W., Cebrià, J., Ribo, S., Pérez-Wienese, R., Vilà, M., Palacios-Marin, I., Fernández-Pérez, A., Vallejo, M., Téllez, N., Rodríguez, M. À., Yanes, O., Lerin, C., Díaz, R., Plosch, T., Tietge, U. J. F., Jimenez-Chillaron, J. C. Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long-term hepatic steatosis and insulin resistance.
    Àrees temàtiques: Saúde coletiva Química Psicología Odontología Nutrição Molecular biology Medicine (miscellaneous) Medicina veterinaria Medicina iii Medicina ii Medicina i Interdisciplinar Genetics General medicine Farmacia Engenharias iv Engenharias ii Educação física Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Ciências ambientais Ciências agrárias i Ciência de alimentos Cell biology Biotecnología Biotechnology Biology Biodiversidade Biochemistry & molecular biology Biochemistry Astronomia / física
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 08926638
    Adreça de correu electrònic de l'autor: oscar.yanes@urv.cat araceli.rodriguez@urv.cat araceli.rodriguez@urv.cat
    Identificador de l'autor: 0000-0003-3695-7157 0000-0002-9456-6528 0000-0002-9456-6528
    Data d'alta del registre: 2024-10-12
    Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
    Enllaç font original: https://faseb.onlinelibrary.wiley.com/doi/full/10.1096/fj.201700717RR
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referència a l'article segons font original: Faseb Journal. 32 (11): fj201700717RR-fj201700717RR
    Referència de l'ítem segons les normes APA: Ramon-Krauel, Marta; Pentinat, Thais; Bloks, Vincent W; Cebria, Judith; Ribo, Silvia; Perez-Wienese, Ricky; Vila, Maria; Palacios-Marin, Ivonne; Ferna (2018). Epigenetic programming at the Mogat1 locus may link neonatal overnutrition with long-term hepatic steatosis and insulin resistance.. Faseb Journal, 32(11), fj201700717RR-fj201700717RR. DOI: 10.1096/fj.201700717RR
    DOI de l'article: 10.1096/fj.201700717RR
    Entitat: Universitat Rovira i Virgili
    Any de publicació de la revista: 2018
    Tipus de publicació: Journal Publications

  • Paraules clau:

    Biochemistry,Biochemistry & Molecular Biology,Biology,Biotechnology,Cell Biology,Genetics,Medicine (Miscellaneous),Molecular Biology
    Weight-gain
    O-acyltransferase 1
    Nutritional epigenetics
    Neonatal overfeeding
    Mouse model
    Monoacylglycerol acyltransferase
    Mice
    Lipid-accumulation
    In-utero
    High-fat diet
    Glucose
    Expression
    Childhood obesity
    Saúde coletiva
    Química
    Psicología
    Odontología
    Nutrição
    Molecular biology
    Medicine (miscellaneous)
    Medicina veterinaria
    Medicina iii
    Medicina ii
    Medicina i
    Interdisciplinar
    Genetics
    General medicine
    Farmacia
    Engenharias iv
    Engenharias ii
    Educação física
    Ciências biológicas iii
    Ciências biológicas ii
    Ciências biológicas i
    Ciências ambientais
    Ciências agrárias i
    Ciência de alimentos
    Cell biology
    Biotecnología
    Biotechnology
    Biology
    Biodiversidade
    Biochemistry & molecular biology
    Biochemistry
    Astronomia / física

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