Linking Microbiota to Human Diseases: A Systems Biology Perspective

Hao Wu, Valentina Tremaroli, F Bäckhed

    87 Citationer (Scopus)

    Abstract

    The human gut microbiota encompasses a densely populated ecosystem that provides essential functions for host development, immune maturation, and metabolism. Alterations to the gut microbiota have been observed in numerous diseases, including human metabolic diseases such as obesity, type 2 diabetes (T2D), and irritable bowel syndrome, and some animal experiments have suggested causality. However, few studies have validated causality in humans and the underlying mechanisms remain largely to be elucidated. We discuss how systems biology approaches combined with new experimental technologies may disentangle some of the mechanistic details in the complex interactions of diet, microbiota, and host metabolism and may provide testable hypotheses for advancing our current understanding of human-microbiota interaction. The gut microbiota is altered in human metabolic diseases. Emerging data show that bacterial functions linked to colonic butyrate production are consistently associated with improved insulin sensitivity, indicating new possible therapeutic avenues. Human metabolic diseases are often associated with decreased diversity and functional richness of the gut microbiota. Modern lifestyles characterized by the widespread use of antimicrobials and consumption of energy-dense foods, additives, and emulsifiers might contribute to loss of microbiota diversity and the increased incidence of chronic diseases. Integration of patient stratification with microbiome functional profiling will be fundamental for the development of personalized medicine. Personal microbiome profiles will be important determinants of the effects of diet and the efficacy of therapeutic drugs.

    OriginalsprogEngelsk
    TidsskriftTrends in Endocrinology and Metabolism
    Vol/bind26
    Udgave nummer12
    Sider (fra-til)758-70
    Antal sider13
    ISSN1043-2760
    DOI
    StatusUdgivet - 1 dec. 2015

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