Pilot study: alterations of intestinal microbiota in obese humans are not associated with colonic inflammation or disturbances of barrier function.

Obesity is associated with low-grade inflammation contributing to insulin-resistance. Gut barrier alterations, described in animal models of obesity, probably favour inflammation. This has not been hitherto described in obese humans. To evaluate gut permeability in asymptomatic obese and its association with plasma (C-reactive protein (CRP), arachidonate/eicosapentaenoate ratio) and faecal (calprotectin and leptin) markers of inflammation and microbiota alterations. A total of 13 obese (age: 33.9 ± 11.5 years; BMI: 35.9 ± 5.0 kg/m²) and 11 control subjects (age: 30.3 ± 8.1 years; BMI: 23.5 ± 2.4 kg/m²) were recruited. Gut permeability was assessed by the lactulose-mannitol-sucralose test, plasma fatty acids by gas chromatography, faecal calprotectin and leptin by Elisa and faecal microbiota by G+C profiling. C-reactive protein was increased in the obese subjects (P = 0.01), but neither the plasma arachidonate/eicosapentaenoate ratio, the faecal levels of calprotectin and leptin, nor the gut permeability were altered. The faecal microbiota was altered in the obese (P = 0.0002), with predominance of bacterial populations having a lower G+C content and decreased concentrations of high G+C populations. Asymptomatic obese individuals with systemic low-grade inflammation do not have evidence of colonic inflammation or gut barrier alteration; however, the biodiversity of their intestinal microbiota is affected. © 2010 Blackwell Publishing Ltd.