Abstract
Type 2 diabetes (T2D) is a chronic metabolic disease characterized by hyperglycemia due to insulin resistance. Mounting evidence has correlated T2D to alterations in the composition of gut microbiota. Accordingly, targeting the gut microbiota has become an emerging strategy for T2D management. The aim of this article is to get a better insight into the rationale for targeting gut microbiota in T2D treatment. Thus, we herein reviewed the change of gut microbiota composition in T2D, factors shaping gut microbiota, and potential mechanisms behind the contribution of gut microbiota to T2D pathogenesis. At present, it has become possible to use intestinal microorganism capsules, bacteria liquid, and other preparations to carry out fecal microbiota transplantation for the treatment and intervention of T2D with insulin resistance and immune-mediated type 1 diabetes.
Highlights
INTRODUCTIONThe level of sugar (glucose) in human blood is under strict control by a hormone known as insulin [1]
The level of sugar in human blood is under strict control by a hormone known as insulin [1]
It enhances the growth of mucin-degrading Akkermansia muciniphila and several short-chain fatty acid (SCFAs)-producing microbiota in the gut of Type 2 diabetes (T2D) patients, which benefits them in maintaining glucose metabolism homeostasis [38]
Summary
The level of sugar (glucose) in human blood is under strict control by a hormone known as insulin [1]. Several human and animal studies emphasized that metformin, a drug commonly used for T2D treatment, altered the gut microbiota composition as well [37] It enhances the growth of mucin-degrading Akkermansia muciniphila and several short-chain fatty acid (SCFAs)-producing microbiota in the gut of T2D patients, which benefits them in maintaining glucose metabolism homeostasis [38]. Patrice et al found that a 4-week high-fat diet led to a 2~3-fold increase in the concentration of plasma LPS, which could be the result of elevated LPS in gut microbiota They found that continuous infusion of LPS in mice triggered a whole-body inflammatory response and insulin resistance in the liver, which suggested the role of LPS signaling in the development of T2D [71]. The transmission of communicable diseases and increased infection risk of FMT need to be addressed
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