期刊
FRONTIERS IN IMMUNOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.594150
关键词
metabolic endotoxemia; lipopolysaccharide; high-fat diet; Toll-like receptor; antimicrobial peptides; gut permeability
类别
资金
- British Heart Foundation (BHF) MRes/PhD Scholarship [FS/17/69/33484]
Diet-induced metabolic endotoxemia can lead to chronic inflammatory conditions due to changes in gut permeability, causing toxins to enter the bloodstream and triggering systemic inflammation. verschiedenen pro-inflammatory cytokines, resulting in chronic low-grade inflammation.
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.
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