The pathological process where lipopolysaccharide (LPS), a potent pro-inflammatory component of the outer membrane of Gram-negative bacteria, crosses a compromised intestinal epithelial barrier and enters the systemic circulation. This translocation, often referred to as “leaky gut,” triggers a widespread, low-grade systemic inflammatory response. The presence of circulating LPS, or endotoxemia, is a major driver of metabolic dysfunction and hormonal resistance.
Origin
This scientific term combines the bacterial molecule Lipopolysaccharide with the physiological concept of Translocation, or movement across a membrane. Its clinical relevance grew exponentially with the recognition that metabolic endotoxemia contributes to insulin resistance and obesity. This pathway provides a tangible link between gut barrier integrity, chronic inflammation, and endocrine health.
Mechanism
Translocation occurs when the tight junctions between enterocytes are disrupted, allowing paracellular passage of LPS into the lamina propria and subsequent entry into the portal and systemic circulation. Once in the blood, LPS binds to the CD14/TLR4 receptor complex on immune cells, initiating the robust release of pro-inflammatory cytokines like TNF-alpha and interleukins. This chronic inflammatory state interferes with insulin signaling and HPA axis regulation, creating a significant endocrine challenge.
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