Articles producció científica> Ciències Mèdiques Bàsiques

Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats

  • Datos identificativos

    Identificador: imarina:5131914
    Autores:
    Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J
    Resumen:
    Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to Type 2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT, and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar-Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma IL-6, PGE2, and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress), and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR, and hypertension is independent of inflammation-mediated IR. The results provide evidence that suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.
  • Otros:

    Autor según el artículo: Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J
    Departamento: Ciències Mèdiques Bàsiques
    Autor/es de la URV: Nogués Llort, Maria Rosa / Romeu Ferran, Marta
    Palabras clave: Obesity Microbiota Hypertension Diabetes microbiota hypertension diabetes
    Resumen: Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to Type 2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT, and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar-Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma IL-6, PGE2, and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress), and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR, and hypertension is independent of inflammation-mediated IR. The results provide evidence that suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.
    Áreas temáticas: Physiology (medical) Physiology Odontología Nutrição Medicine (all) Medicina ii Medicina i General medicine Farmacia Endocrinology, diabetes and metabolism Endocrinology & metabolism Educação física Ciências biológicas ii Ciências biológicas i Biotecnología
    Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 15221555
    Direcció de correo del autor: marta.romeu@urv.cat
    Identificador del autor: 0000-0002-2131-1858
    Fecha de alta del registro: 2024-09-07
    Versión del articulo depositado: info:eu-repo/semantics/submittedVersion
    Enlace a la fuente original: https://journals.physiology.org/doi/full/10.1152/ajpendo.00323.2017
    URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referencia al articulo segun fuente origial: American Journal Of Physiology-Endocrinology And Metabolism. 314 (6): E552-E563
    Referencia de l'ítem segons les normes APA: Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J (2018). Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats. American Journal Of Physiology-Endocrinology And Metabolism, 314(6), E552-E563. DOI: 10.1152/ajpendo.00323.2017
    DOI del artículo: 10.1152/ajpendo.00323.2017
    Entidad: Universitat Rovira i Virgili
    Año de publicación de la revista: 2018
    Tipo de publicación: Journal Publications
  • Palabras clave:

    Endocrinology & Metabolism,Endocrinology, Diabetes and Metabolism,Physiology,Physiology (Medical)
    Obesity
    Microbiota
    Hypertension
    Diabetes
    microbiota
    hypertension
    diabetes
    Physiology (medical)
    Physiology
    Odontología
    Nutrição
    Medicine (all)
    Medicina ii
    Medicina i
    General medicine
    Farmacia
    Endocrinology, diabetes and metabolism
    Endocrinology & metabolism
    Educação física
    Ciências biológicas ii
    Ciências biológicas i
    Biotecnología
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