Oral Presentation Australian & New Zealand Obesity Society 2016 Annual Scientific Meeting

Increased intestinal permeability as a risk factor for type 2 diabetes in obesity (#52)

Amanda J Cox 1 2 , Ping Zhang 1 2 , Donald W Bowden 3 , Benedict Devereaux 4 , Peter M Davoren 5 , Allan W Cripps 1 2 , Nicholas P West 1 2
  1. Menzies Health Institute Queensland, Southport, QLD, Australia
  2. Griffith University, Southport, QLD, Australia
  3. Centre for Diabetes Research, Wake Forest School of Medicine, Winston-Salem, NC, USA
  4. Digestive Diseases QLD, Chermside, QLD, Australia
  5. Diabetes and Endocrinology, Gold Coast University Hospital, Southport, QLD, Australia

Introduction: The interplay between the gut microbiota, intestinal permeability and chronic low grade inflammatory responses in the context of risk for obesity-associated disease continue to be of interest. A permeable intestinal mucosa is necessary to facilitate critical absorptive functions, but alterations in intestinal permeability have the potential to trigger Metabolic Endotoxaemia (ME) which may result in downstream activation of inflammatory signalling pathways and contribute to risk for disease. The aim of the study was to examine the associations between intestinal permeability and type 2 diabetes (T2D) using a derived risk score approach. Methods: A total of 130 individuals with T2D (age: 57.5±6.2 years (mean ± SD); BMI: 30.4±3.2; 45% female) and 161 individuals without T2D (age: 37.4±12.5 years; BMI: 25.1±3.9; 65% female) were included in the study. Assessment of intestinal permeability included measurement of circulating lipopolysaccharide (LPS), LPS-binding protein (LBP) and intestinal fatty acid binding protein (iFABP) concentrations which were then used for calculation of a derived permeability risk score (PRS) based on quartile scoring of each individual measure. Associations between the PRS and T2D status were assessed using logistic regression models. Results: LBP (~34%, p<0.001), iFABP (~46%, p<0.001) and the PRS (~24% p<0.001) were all significantly higher in the T2D affected individuals. Quantification of risk across PRS tertiles revealed that individuals with a PRS in the upper tertile were 5.07 times more likely (CI: 1.72-14.95; p=0.003) to have T2D independent of age, sex and BMI. Conclusions: These data support an association between intestinal permeability and risk for T2D. Consideration of intestinal permeability assessment as a potential tool for classifying individuals with Metabolic Syndrome as high or low risk for T2D development appears a logical progression of this work.