Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors

Lipopolysaccharide binding protein, obesity status and incidence of metabolic syndrome: a prospective study among middle-aged and older Chinese

“…Likewise, a recent cross-sectional study in 420 Spanish individuals also indicated that higher LBP was associated with MetS and its components, including central obesity and low HDL-cholesterol [12]. However, the cross-sectional nature of previous studies could lead to reverse causation, since common symptoms of MetS may also alter gastrointestinal conditions and promote occurrence of subclinical endotoxaemia [10,11]. With a prospective design, our current analyses provided stronger evidence to support the putative contributions of endotoxaemia to the development of metabolic abnormalities.…”

“…On the other hand, the components of MetS, such as hypertriacylglycerolaemia, hyperglycaemia and hyperinsulinaemia, have been hypothesised to contribute to endotoxaemia through altering jejunal motility and gastrointestinal transit time, conditions that may favour bacterial overgrowth and leak endotoxins into the intestinal mucosa [10,11]. Whether endotoxaemia predisposes to the onset of metabolic deterioration in free-living populations remains to be elucidated.…”

Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent

“…intestinal epithelium during obesity in both humans and rodents (6,12,46), and it has been hypothesized that decreased barrier function leads to passage of microbial components, such as lipopolysaccharide (LPS), which drives systemic inflammation (5). However, the precise defects in gut barrier function and the possible role played in the development of obesity remain unclear.…”

“…However, the precise defects in gut barrier function and the possible role played in the development of obesity remain unclear. Measurement of intestinal permeability in vivo has been useful to show impaired intestinal permeability (12,46), yet these approaches do not identify the site of the defect. The only study using an ex vivo intestinal permeability test to compare different sections of the gut was performed once obesity was established (43), not during development of the obese phenotype.…”

Nonalcoholic fatty liver disease as trigger of cardiovascular and metabolic complication in metabolic syndrome

“…This suggests that gut microbiota might lead to human metabolic abnormalities by triggering chronic inflammation through LPS invasion [70]. On the other hand, the components of MS, such as hypertriacylglycerolaemia, hyperglycaemia and hyperinsulinaemia, are hypothesized to contribute to endotoxaemia through altering jejunal motility and gastrointestinal transit time, conditions that may favor bacterial overgrowth, and leak endotoxins into the intestinal mucosa [71]. This might also explain the increased prevalence of SIBO in NAFLD patients, as reported by our group [25].…”