Reduced Lipopolysaccharide-Binding Protein (LBP) Levels Are Associated with Non-Alcoholic Fatty Liver Disease (NAFLD) and Adipose Inflammation in Human Obesity

Figures

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  Figure 1. Images showing liver histology of two representative study participants with (A) non-alcoholic fatty liver disease (NAFLD) or (B) normal liver. Patient (A): NAFLD (NAS) activity score: 4, staging: 0; SAF score: steatosis: 3, ballooning: 0, lobular inflammation: 0. Patient (B): normal liver tissue. Images viewed under ×200 magnification; hematoxylin and eosin staining.

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  Figure 2. Serum LBP concentration in relation to NAS score for lobular inflammation in liver biopsy. * Spearman’s coefficient. Abbreviations: LBP: lipopolysaccharide-binding protein; NAS: NASH activity score.

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  Figure 3. Number of CD68+ cells infiltrating the VAT in relation to serum LBP subgroup. Mean ± standard error. Mann–Whitney test was calculated. Abbreviations: LBP: lipopolysaccharide-binding protein; VAT: visceral adipose tissue.

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  Figure 4. Potential mechanisms associating lower lipopolysaccharide-binding protein (LBP) levels with dysmetabolic conditions in obesity. In obesity, bacterial overgrowth and LPS release into the portal vein trigger systemic inflammation and stimulate pro-inflammatory responses in the liver, resulting in an increased risk of metabolic diseases and NAFLD. LBP may improve hepatic LPS clearance and hide LPS from recognition by TLR4+ macrophages, thus protecting individuals from obesity-associated metabolic disturbances. Dotted arrows show potential metabolic pathways linking LBP levels to metabolic disease in obesity. Abbreviations: NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; LPS: lipopolysaccharide; LBP: LPS-binding protein; HbA1c: glycosylated hemoglobin; FBG: fasting blood glucose.