PRJNA723003
Characterization of the Fecal Microbiome in Dogs with Diabetes Mellitus
Diabetes mellitus in humans has been associated with a significant gastrointestinal dysbiosis, which exacerbates the condition by inducing low-level systemic inflammation, insulin resistance, excess nutrient absorption, and aberrant energy utilization. Although the fecal microbiome has been investigated in other canine diseases, bacterial changes have yet to be explored in dogs with diabetes mellitus. Therefore, the goals of this pilot study were to (1) to evaluate changes in fecal microbiota over time in newly diagnosed diabetic dogs as their disease becomes regulated and (2) to determine whether quantitative aspects of the fecal microbiome correlate with serum fructosamine and other markers of diabetic control. Six dogs with newly diagnosed diabetes were recruited from various primary care veterinary hospitals. Dogs were be screened for other systemic diseases via history, physical exam, and blood/urine analyses. At the time of diagnosis (week 0) and every 2 weeks for the first 12 week of treatment, diabetic status was evaluated by owner and clinician questionnaires and serum fructosamine. At each timepoint, a rectal swab was collected for microbial analysis. Bacterial DNA will be extracted and the 16S gene amplified using the Fluidigm Access Array and sequenced on the Illumina MiSeq platform. Taxa relative abundances, alpha diversity, and beta diversity were examined for changes with time and associated with fructosamine and clinical parameters of diabetic control. Characterization of the fecal microbiome during treatment of canine diabetes mellitus will pave the way for future investigations of non-insulin adjunctive therapies that alter the gastrointestinal microbiome (e.g., diet, prebiotics, probiotics, fecal microbiota transfer), which have been shown to improve insulin sensitivity and disease regulation in human diabetics. Furthermore, understanding the gastrointestinal microbial changes in canine diabetes may provide clues to the pathogenesis of this disease, which is currently poorly understood.