Gut Microbiota, Probiotics and Diabetes

Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal
microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from
the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin
receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins
within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic
β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in
animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis
of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence
suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of
adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes.