MON-177 The Effect of Gluten Protein Components on Type 1 Diabetes and the Viability of Treatment with Antioxidants

Abstract

Type one diabetes (T1D) is an autoimmune disease of the pancreas in which a T-cell mediated destruction of the insulin-producing islet Langerhans (Atkinson, Eisenbarth, & Michels, 2013). It has been found to link with celiac disease (CD), a gluten-sensitive autoimmune enteropathy where the lining of the small intestine atrophies and the tight junctions breakdown allowing the immunogenic protein component of gluten, gliadin into the bloodstream. This effect has been documented in people with and without CD. Analogous proteins to gliadin can be found in other cereal grains and can also instigate the autoimmune response characterized in celiac (Schalk, Lexhaller, Koehler, & Scherf, 2017). This study will attempt to connect proteins analogous to gliadin to the immune response in both diseases and attempt to treat any observed negative effects. Pancreatic 1.1B4 cells were cultured and treated with concentrations of gliadin (0.4-3.2 mg/mL)in ethanol, and concentrations of secalin (.18-.72 mg/mL), a rye-derived analogue to gliadin. Concentrations of the proteins were chosen to simulate the ratio of the proteins found in the respective grains, so approximately 2.3 parts gliadin to 1 part secalin (Schalk, Lexhaller, Koehler, & Scherf, 2017). Gliadin increased viability significantly while secalin decreased viability. Further analysis determined gliadin increased insulin production (P<0.01). Secalin decreased insulin production significantly at high concentrations. An IL-6 ELISA determined that gliadin significantly increased IL-6 production linearly. Results of IL-6 production for secalin show a significant linear decreasing trend. Oxidative effects of gliadin and secalin were measured. Gliadin appeared to significantly increase the oxidative stress of the cells. The secalin also increased the oxidative stress though it was a linearly decreasing trend. The antioxidant beta carotene (BC)was added to the treatment to determine if the negative oxidative effects and the cytokine production could be decreased. Data shows that adding BC to the gliadin treatment significantly decreased the oxidative stress and the cytokine production and significantly increased cell viability and insulin production. BC in secalin decreased oxidative stress compared to the secalin concentrations. It also increased insulin production significantly (p<0.01)at lower concentrations. However, secalin and BC solutions had little effect on viability, and it displayed higher values of IL-6 production suggesting that BC may promote a proinflammatory response as described in other studies (Obermüller-Jevic, Schlegel, Flaccus, & Biesalski, 2001). This suggests that BC can reduce some negative effects found in the gliadin and secalin treatment, suggesting potential treatments for those who have T1D. Further research is being conducted to confirm the benefits of antioxidants on T1D.