| Literature DB >> 33505393 |
Shireen Mohammad1, Christoph Thiemermann1.
Abstract
Diet-induced metabolic endotoxemia is an important factor in the development of many chronic diseases in animals and man. The gut epithelium is an efficient barrier that prevents the absorption of liposaccharide (LPS). Structural changes to the intestinal epithelium in response to dietary alterations allow LPS to enter the bloodstream, resulting in an increase in the plasma levels of LPS (termed metabolic endotoxemia). LPS activates Toll-like receptor-4 (TLR4) leading to the production of numerous pro-inflammatory cytokines and, hence, low-grade systemic inflammation. Thus, metabolic endotoxemia can lead to several chronic inflammatory conditions. Obesity, diabetes, and non-alcoholic fatty liver disease (NAFLD) can also cause an increase in gut permeability and potential pharmacological and dietary interventions could be used to reduce the chronic low-grade inflammation associated with endotoxemia.Entities:
Keywords: Toll-like receptor; antimicrobial peptides; gut permeability; high-fat diet; lipopolysaccharide; metabolic endotoxemia
Mesh:
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Year: 2021 PMID: 33505393 PMCID: PMC7829348 DOI: 10.3389/fimmu.2020.594150
Source DB: PubMed Journal: Front Immunol ISSN: 1664-3224 Impact factor: 7.561