The immunity-diet-microbiota axis in the development of metabolic syndrome

E. Brandsma, Tom Houben, J. Fu, Ronit Shiri-Sverdlov, M. Hofker*

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    Abstract

    PURPOSE OF REVIEW: Recent evidence demonstrates that the gut-microbiota can be considered as one of the major factors causing metabolic and cardiovascular diseases. RECENT FINDINGS: Pattern recognition receptors as well as antimicrobial peptides are a key factor in controlling the intestinal microbiota composition. Deficiencies in these genes lead to changes in the composition of the gut-microbiota, causing leakage of endotoxins into the circulation, and the development of low-grade chronic inflammation and insulin resistance. Dietary composition can also affect the microbiota: a diet rich in saturated fats allows the expansion of pathobionts that damage the intestinal epithelial cell layer and compromise its barrier function. In contrast, a diet high in fiber supports the microbiota to produce short-chain fatty acids, thereby promoting energy expenditure and protecting against inflammation and insulin resistance. SUMMARY: The interactions between the microbiota, innate immunity, and diet play an important role in controlling metabolic homeostasis. A properly functioning innate immune system, combined with a low-fat and high-fiber diet, is important in preventing dysbiosis and reducing the susceptibility to developing the metabolic syndrome and its associated cardiovascular diseases.
    Original languageEnglish
    Pages (from-to)73-81
    Number of pages9
    JournalCurrent Opinion in Lipidology
    Volume26
    Issue number2
    DOIs
    Publication statusPublished - Apr 2015

    Keywords

    • endotoxemia
    • innate immunity
    • metabolic syndrome
    • microbiota
    • short-chain fatty acids
    • CHAIN FATTY-ACIDS
    • GUT MICROBIOTA
    • INTESTINAL MICROBIOTA
    • INSULIN SENSITIVITY
    • RECEPTOR
    • MICE
    • PROMOTES
    • MUCOSAL
    • DYSBIOSIS
    • OBESITY

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