2 research outputs found

    New Insights into Alleviating Diabetes Mellitus: Role of Gut Microbiota and a Nutrigenomic Approach

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    The scientific literature has shown that diet is able to modify the gut microbiota and contribute to obesity and diabetes development. This process—characterized by inflammation and gut barrier disruption—can affect the immune system and alter the adipogenesis and insulin resistance. This chapter describes the advances in nutrigenomics and Human Intestinal Microbiota (HIM) modification, and its relation with diabetes mellitus type two (DM2). In context where health and feeding are the main concerns of the human being, food innovation takes a special interest to people that look for a healthy diet or demand a functional aliments, such as nutraceutical. Some products derived from diet and interaction with HIM module the expression of many genes on the host, the so-called epigenome, with favorable effects. Novel functional fiber like low-glycemic oligosaccharides and sweeteners shows a potential prebiotic activity giving a new focus of nutritional guidelines for control and prevention of DM2. The use of prebiotics derived from functional fiber sources, such as fructo-oligosaccharides and beta-glucans as well as lignin and keffir, can contribute to the development of a healthy HIM by promoting the growth of specific bacteria, some of them associated with the prevention of obesity and diabetes

    The Microbiome and the Epigenetics of Diabetes Mellitus

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    Gut microbiota (GM) in the epigenetic mechanisms of diabetes mellitus and the reprogramming of the cells is a novel and emerging concept. The purpose of this chapter is to describe the modification of the GM and its relation with DM2. The increased risk of this disease is associated with changes in the amount of Bacteroides/Clostridium in the Firmicutes/Bacteroidetes ratio of people having DM. A dysbiosis state associated generates low-grade inflammation with similar characteristics that occur under metabolic syndrome, whose pattern is recognized by Toll-like receptor that recognizes important patterns of immunity. The synthesis of butyrate generated by intestinal microorganisms inhibits the metabolic pathway of histone deacetylase, promoting cellular differentiation, proliferation, and insulin resistance. On the other hand, the direct relationship between the neuroendocrine system and the GM has been demonstrated through the production of serotonin by enterochromaffin cells, whose action could influence the etiopathogenic factors of DM2
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