Articles producció científica> Ciències Mèdiques Bàsiques

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

  • Dades identificatives

    Identificador: imarina:5131914
    Autors:
    Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J
    Resum:
    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.
  • Altres:

    Autor segons l'article: Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J
    Departament: Ciències Mèdiques Bàsiques
    Autor/s de la URV: Nogués Llort, Maria Rosa / Romeu Ferran, Marta
    Paraules clau: Obesity Microbiota Hypertension Diabetes microbiota hypertension diabetes
    Resum: 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.
    Àrees temàtiques: 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
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 15221555
    Adreça de correu electrònic de l'autor: marta.romeu@urv.cat
    Identificador de l'autor: 0000-0002-2131-1858
    Data d'alta del registre: 2024-09-07
    Versió de l'article dipositat: info:eu-repo/semantics/submittedVersion
    Enllaç font original: https://journals.physiology.org/doi/full/10.1152/ajpendo.00323.2017
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referència a l'article segons font original: American Journal Of Physiology-Endocrinology And Metabolism. 314 (6): E552-E563
    Referència 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 de l'article: 10.1152/ajpendo.00323.2017
    Entitat: Universitat Rovira i Virgili
    Any de publicació de la revista: 2018
    Tipus de publicació: Journal Publications
  • Paraules clau:

    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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