The gut-pancreas axis: microbial dysbiosis as a pathogenic driver of diabetes and pancreatic cancer.

The gut microbiome dysbiosis is a potential contributing mediator for the gut and pancreas link. The gut microbiome contributes to the development of both diabetes and pancreatic cancer. There are approximately two distinct ways through which the gut microbiome leads to cell damage and then systemic inflammatory responses. The gut microbiome generates a unique set of metabolic products, activating diverse pathways and cytokines. The bottom line for this process leads to the generation of systemic inflammation. In type 2 diabetes, inflammatory signaling predominantly disrupts IRS-1/PI3K/AKT signaling, impairing insulin receptor pathways and glucose absorption, triggering β-cell malfunction and insulin resistance. Dysbiosis-associated inflammatory signaling in pancreatic cancer stimulates the growth of the tumour via activating oncogenic pathways, immune evasion, and epithelial-mesenchymal transition (EMT). The bacterial metabolites can cause. DNA mutations and affect the signaling pathways of cancer cells. In addition, this review offers an integrated microbiome-driven inflammatory-metabolic paradigm utilizing the gut-pancreas axis to associate pancreatic cancer and diabetes. A realistic and in-depth understanding of the above-described processes could result in the development of new techniques for the targeted modification of the gut microbiome for the prevention and management of such diseases.