In persons with type 1 diabetes, increased intestinal inflammation, reduced gut barrier function and resulting influx of proinflammatory molecules have been described. This might contribute to systemic inflammation and the development of diabetic complications like nephropathy and cardiovascular disease. Interestingly, the gut microbiota is altered in persons with type 1 diabetes, who have less butyrate-producing bacteria. The short-chain fatty acid butyrate improves the intestinal barrier function, and the altered bacterial composition is hypothesized to play a role in the intestinal inflammation. Treatment with butyrate has improved metabolic, colonic and renal function in animal models of chronic kidney disease.
Persons with type 1 diabetes and albuminuria are recruited from Steno Diabetes Center Copenhagen and Folkhälsan Research Center, FinnDiane, Helsinki, Finland and screened for intestinal inflammation. 48 participants with intestinal inflammation (fecal calprotectin ≥50 μg/g) are randomized to receive 3.6 g sodium butyrate or placebo for 12 weeks.
- Primary endpoint: The effect of sodium butyrate on fecal calprotectin level.
- Secondary endpoints: The effect of sodium butyrate on fecal intestinal alkaline phosphatase activity, short-chain fatty acids, kidney function and albuminuria.
- Tertiary endpoints: The effect of the intervention on other markers of inflammation, endothelial dysfunction, serum lipids, autonomic nervous system function and gastrointestinal symptoms. Impact of specific genetic variants on clinical phenotypes and on the effect of the intervention.
We aim to test whether orally ingested sodium butyrate can reduce intestinal inflammation in persons with type 1 diabetes and albuminuria by conducting a randomized, placebo-controlled, double-blind, two-site trial.
Folkhälsan Research Center, FinnDiane, Helsinki, Finland