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Abstract
Type 2 diabetes (T2D) has been linked with increased intestinal permeability, but the clinical significance of this phenomenon remains unknown. The objective of this study was to investigate the potential link between glucose control, intestinal permeability, diet and intestinal microbiota in patients with T2D. Thirty‐two males with well‐controlled T2D and 30 age‐matched male controls without diabetes were enrolled in a case–control study. Metabolic parameters, inflammatory markers, endotoxemia, and intestinal microbiota in individuals subdivided into high (HP) and normal (LP) colonic permeability groups, were the main outcomes. In T2D, the HP group had significantly higher fasting glucose (P = 0.034) and plasma nonesterified fatty acid levels (P = 0.049) compared with the LP group. Increased colonic permeability was also linked with altered abundances of selected microbial taxa. The microbiota of both T2D and control HP groups was enriched with Enterobacteriales. In conclusion, high intestinal permeability was associated with poorer fasting glucose control in T2D patients and changes in some microbial taxa in both T2D patients and nondiabetic controls. Therefore, enrichment in the gram‐negative order Enterobacteriales may characterize impaired colonic permeability prior to/independently from a disruption in glucose tolerance.
Highlights
Impaired barrier function has been hypothesized to lead to the increased uptake of antigens of both dietary and bacterial origin from the intestinal lumen into the circulation, activating the innate immune system (Cani and Everard 2016)
As the density of bacteria is highest in the colon we explored whether clinical parameters, dietary intakes (Tables 3 and 4) and intestinal bacterial abundances (Fig. 4) differed between those with high and normal colonic permeability
In this study we have measured markers of glucose tolerance, inflammation, endotoxemia, intestinal permeability, and intestinal bacterial community structure in the same individuals, investigating for the first time whether there is a potential link between intestinal permeability and glucose control/inflammation in Type 2 diabetes (T2D), as a first translation from the extensive and seemingly consistent animal literature
Summary
Impaired barrier function has been hypothesized to lead to the increased uptake of antigens of both dietary and bacterial origin from the intestinal lumen into the circulation, activating the innate immune system (Cani and Everard 2016). Increased fat content of the diet is associated with dysbiosis and increased circulating lipopolysaccharide (LPS), called metabolic endotoxemia and this has been associated with changes in the gut barrier function in mice (Cani et al 2008, 2009; Kim et al 2012). TLR-4 activation leads to increased levels of proinflammatory cytokines, such as TNF-a and interleukins, and this systemic low-grade inflammation is associated with insulin resistance (Cani et al 2007). Administering LPS to animals and humans increases inflammatory markers and insulin resistance, corroborating a role for LPS in metabolic diseases characterized by low-grade inflammation (Cani et al 2007; Andreasen et al 2010, 2011)
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