What is the Origin of Lipopolysaccharide Endotoxemia?

This term is rooted in microbiology and toxicology, where 'lipopolysaccharide' identifies the molecule and 'endotoxemia' denotes its presence in the blood, causing systemic toxicity. The primary source is often intestinal permeability, or 'leaky gut,' which allows bacterial fragments to translocate across the epithelial barrier. Recognition of this pathway has become central to understanding the gut-hormone and gut-brain axes.

What is the Mechanism of Lipopolysaccharide Endotoxemia?

Once LPS enters the bloodstream, it binds to the CD14/TLR4 receptor complex on immune cells, particularly monocytes and macrophages. This binding activates the NF-κB signaling pathway, leading to the massive transcription and release of pro-inflammatory cytokines, such as TNF-alpha and IL-6. This systemic inflammation interferes with insulin signaling in peripheral tissues, promotes hepatic fat deposition, and disrupts the hypothalamic-pituitary axis, thereby linking gut barrier integrity directly to endocrine and metabolic health.

Lipopolysaccharide Endotoxemia

Meaning

Lipopolysaccharide endotoxemia describes the clinical state characterized by the presence of elevated levels of lipopolysaccharide (LPS), a major component of the outer membrane of Gram-negative bacteria, in the systemic circulation. LPS is a potent endotoxin that, when it breaches the intestinal barrier, triggers a robust, systemic inflammatory and immune response. Clinically, this low-grade, chronic endotoxemia is a significant driver of metabolic dysfunction, insulin resistance, and chronic inflammatory diseases.

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HRTioJuly 20, 2025

Lipopolysaccharide Endotoxemia

Meaning

Origin

Mechanism

Gut Microbiome Your Metabolic Engine

Are There Biomarkers Indicating Gut-Mediated Hormone Receptor Insensitivity?

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