Articles producció científica> Ciències Mèdiques Bàsiques

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

  • Identification data

    Identifier: imarina:5131914
    Authors:
    Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J
    Abstract:
    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.
  • Others:

    Author, as appears in the article.: Ramos-Romero S, Hereu M, Atienza L, Casas J, Jáuregui O, Amézqueta S, Dasilva G, Medina I, Nogués M, Romeu M, Torres J
    Department: Ciències Mèdiques Bàsiques
    URV's Author/s: Nogués Llort, Maria Rosa / Romeu Ferran, Marta
    Keywords: Obesity Microbiota Hypertension Diabetes microbiota hypertension diabetes
    Abstract: 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.
    Thematic Areas: 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
    licence for use: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 15221555
    Author's mail: marta.romeu@urv.cat
    Author identifier: 0000-0002-2131-1858
    Record's date: 2024-09-07
    Papper version: info:eu-repo/semantics/submittedVersion
    Link to the original source: https://journals.physiology.org/doi/full/10.1152/ajpendo.00323.2017
    Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
    Papper original source: American Journal Of Physiology-Endocrinology And Metabolism. 314 (6): E552-E563
    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
    Article's DOI: 10.1152/ajpendo.00323.2017
    Entity: Universitat Rovira i Virgili
    Journal publication year: 2018
    Publication Type: Journal Publications
  • Keywords:

    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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