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Impaired intestinal barrier and tissue bacteria: Pathomechanisms for metabolic diseases.
Front. Endocrin. 12:616506 (2021)
An intact intestinal barrier, representing the interface between inner and outer environments, is an integral regulator of health. Among several factors, bacteria and their products have been evidenced to contribute to gut barrier impairment and its increased permeability. Alterations of tight junction integrity - caused by both external factors and host metabolic state - are important for gut barrier, since they can lead to increased influx of bacteria or bacterial components (endotoxin, bacterial DNA, metabolites) into the host circulation. Increased systemic levels of bacterial endotoxins and DNA have been associated with an impaired metabolic host status, manifested in obesity, insulin resistance, and associated cardiovascular complications. Bacterial components and cells are distributed to peripheral tissues via the blood stream, possibly contributing to metabolic diseases by increasing chronic pro-inflammatory signals at both tissue and systemic levels. This response is, along with other yet unknown mechanisms, mediated by toll like receptor (TLR) transduction and increased expression of pro-inflammatory cytokines, which in turn can further increase intestinal permeability leading to a detrimental positive feedback loop. The modulation of gut barrier function through nutritional and other interventions, including manipulation of gut microbiota, may represent a potential prevention and treatment target for metabolic diseases.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Review
Schlagwörter
Adipose Tissue Microbiota ; Endotoxemia ; Intestinal Permeability ; Metabolic Disease ; Microbiome ; Obesity ; Type 2 Diabetes ; Zonulin
ISSN (print) / ISBN
1664-2392
e-ISSN
1664-2392
Zeitschrift
Frontiers in Endocrinology
Quellenangaben
Band: 12,
Artikelnummer: 616506
Verlag
Frontiers
Verlagsort
Lausanne
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen
Universitat Leipzig
German Research Foundation (DFG)
Deutsche Forschungsgemeinschaft (DFG, German Research foundation)
German Research Foundation (DFG)
Deutsche Forschungsgemeinschaft (DFG, German Research foundation)