Abstract

Lipopolysaccharide (LPS; endotoxin) is a lipophilic pathogenic factor derived from gut Gram-negative bacteria. Increased serum LPS concentrations are associated with the metabolic syndrome, termed metabolic endotoxemia. Since the origin of circulating LPS is the gut lumen, we studied the mechanisms of LPS transport across the gut mucosa, hypothesizing that transport occurs via known lipid uptake pathways. Since glucagon-like peptide-2 (GLP-2) reduces intestinal solute permeability but enhances fat absorption, we also hypothesized that GLP-2 affects LPS transport during fat absorption. We thus examined LPS transport mechanisms and the effect of exogenous GLP-2 on LPS transport in intact intestinal tissues in vitro and in vivo.

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