Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection

Sara Federici Microbiota 2018Dr. Sara Federici from Weizmann Institute of Science, Israel will join the Porto Microbiota 2018 Congress which will be held in October 28-30, 2018, at Porto, Portugal and will talk about "Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection".

"Obesity, glucose intolerance, hyperglycemia and diabetes are related disorders associated with the metabolic syndrome. Our lab recently showed that systemic hyperglycemia in obese and diabetic mice causes enhanced intestinal epithelial permeability, driven by dysfunction of epithelial tight junctions, leading to increased dissemination of enteric pathogens. Our in vivo observations showed that damage to the tight junctions between the intestinal epithelial cells directly correlated with higher glucose concentrations and prolonged exposure time to high glucose levels. Moreover, insulin injection to diabetic mice led to controlled glycemic response and resulted in normal intestinal barrier function and systemic resistance to bacterial infection. We found that hyperglycemia-induced intestinal barrier breakdown is driven by the intestinal glucose transporter GLUT2. Mice with epithelial–specific GLUT2 ablation had intact tight and adherence junction complexes, showed protection against high serum glucose levels and significant resistance to systemic dissemination of enteric pathogens. In healthy human patients, a strong correlation was found between individualized glycemic control, indicated by glycated hemoglobin levels, and the concentration of intestinal bacterial ligands in the blood. Our data shows a causative link between hyperglycemia and the loss of intestinal barrier integrity. We suggest that gut-related infection and inflammation may help to explain the mechanisms driving chronic low-grade inflammation found in obese and type 2 diabetes patients."


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