Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models

Authors

  • Maria E. Meneses,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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    • These authors contributed equally to this work.

  • Antonio Camargo,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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    • These authors contributed equally to this work.

  • Pablo Perez-Martinez,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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  • Javier Delgado-Lista,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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  • Cristina Cruz-Teno,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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  • Yolanda Jimenez-Gomez,

    1. Department of Cell Biology, Physiology and Immunology, University of Cordoba, Cordoba, Spain
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  • Juan A. Paniagua,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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  • Francisco M. Gutierrez-Mariscal,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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  • Francisco J. Tinahones,

    1. Hospital Virgen de la Victoria, Malaga, CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Spain
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  • Antonio Vidal-Puig,

    1. Metabolic Research Laboratories, Institute of Metabolic Science, University of Cambridge, Cambridge, UK
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  • Helen M. Roche,

    1. Nutrigenomics Research Group, School of Public Health, UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin, Ireland
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  • Francisco Perez-Jimenez,

    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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  • Maria M. Malagon,

    1. Department of Cell Biology, Physiology and Immunology, University of Cordoba, Cordoba, Spain
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    • These authors contributed equally to this work.

  • Jose Lopez-Miranda

    Corresponding author
    1. Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
    • Lipids and Atherosclerosis Unit at Reina Sofia University Hospital, Avda. Menendez Pidal, s/n. 14004-Córdoba, Spain Fax: +34-957218250
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    • These authors contributed equally to this work.


Abstract

Scope: Dysfunctional adipose tissue may be an important trigger of molecular inflammatory pathways that cause cardiovascular diseases. Our aim was to determine whether the specific quality and quantity of dietary fat produce differential postprandial inflammatory responses in adipose tissue from metabolic syndrome (MetS) patients.

Methods and results: A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to 1 of 4 diets: (i) high-saturated fatty acid (HSFA), (ii) high-monounsaturated fatty acid (HMUFA), (iii) low-fat, high-complex carbohydrate diet supplemented with n−3 polyunsaturated fatty acids (PUFA) (LFHCC n−3), and (iv) low-fat, high-complex carbohydrate diet supplemented with placebo (LFHCC), for 12 wk each. A fat challenge reflecting the fatty acid composition as the original diets was conducted post-intervention. We found that p65 gene expression is induced in adipose tissue (p=0.003) at the postprandial state. In addition, IκBα (p<0.001), MCP-1 (p<0.001) and IL-1β (p<0.001) gene expression was equally induced in the postprandial state, regardless of the quality and quantity of the dietary fat. Notably, IL-6 transcripts were only detected in the postprandial state.

Conclusions: Our results indicate that individuals with MetS typically exhibit exacerbated adipose tissue postprandial inflammatory responses, which seem to be independent of the quality and quantity of dietary fat.

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