Targeting Gut Microbiota for the Prevention of mitochondrial dysfunction and Control of Diabetes.

This study is focused on understanding the of the role of gut microbial metabolites on the mitochondria function and how may affect immune-metabolic regulation, insulin secretion and insulin resistance associated with T2D. This is a novel approach to understand the effects of diet-induced obesity and T2D, since "metabolite sensors" have not been explored as molecules responsible for driving the metabolic syndrome. Diet and gut microbiota is now a leading suspect for the increased incidence of diabetes in western countries. We believe that low intake of dietary fiber in western countries leads to an altered microbiota, altered gut homeostasis and increased exposure to microbial pathogens, resulting in inflammation of the adipocyte tissues, affecting mitochondrial function and therefore cell/organ failure. If diet/microbiota does underlie the development of T2D in humans, then assessment of the mechanisms whereby microbial metabolites through their sensing receptors may influence mitochondria plasticity, particularly in T2D, will be a new avenue of investigation to understand disease pathogenesis. This could lead to new strategies to prevent or treat T2D.