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Figure 2

The gut epithelium is an efficient barrier that prevents absorption of LPS derived from Gram-negative gut microbiota. Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia. Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption and plasmatic levels. LPS in the bloodstream is transported by lipoproteins and LBP. In the liver, LPS is cleared by hepatocytes and excreted in the bile. LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease. In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression. In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines. Full color version of this figure available via http://dx.doi.org/10.1530/JME-13-0079

This Article

  1. J Mol Endocrinol vol. 51 no. 2 R51-R64