Page 13 - Introduction to FMT
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FMT Introduction





         This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-
         Commercial No Derivatives License, which permits for noncommercial use, distribution, and reproduction
         in any digital medium, provided the original work is properly cited and is not altered in any way.


         Abstract


         The worldwide prevalence of metabolic syndrome, which includes obesity and its associated diseases, is
         rising rapidly. The human gut microbiome is recognized as an independent environmental modulator of
         host metabolic health and disease. Research in animal models has demonstrated that the gut
         microbiome has the functional capacity to induce or relieve metabolic syndrome. One way to modify the
         human gut microbiome is by transplanting fecal matter, which contains an abundance of live
         microorganisms, from a healthy individual to a diseased one in the hopes of alleviating illness. Here we
         review recent evidence suggesting efficacy of fecal microbiota transplant (FMT) in animal models and
         humans for the treatment of obesity and its associated metabolic disorders.



         Keywords: Fecal microbiota transplant, metabolic syndrome, obesity


         Introduction


         Over the past half-century, the prevalence of obesity and its related metabolic disorders, such as type 2
         diabetes (T2D), non-alcoholic fatty liver disease, and hypercholesterolemia, have increased dramatically.
         Collectively, these diseases cause an undue burden on health care costs and significant morbidity and
         mortality. While these diseases are linked to human genetics and lifestyle changes, the human gut
         microbiome, or the microorganisms living in the gut and their collective genomes, is now recognized to
         play an emerging role in metabolic health and disease [1,2]. Trillions of diverse organisms, including
         bacteria, fungi, archaea, and viruses, have co-evolved to live in the human gut [3]. These commensal
         organisms comprise the gut microbiome, and their collective genome, referred to as the metagenome,
         contains more than a hundred-fold the number of genes than their host does [4]. Certain metagenomic
         patterns are associated with obesity, as well as other phenotypes [5]. These patterns are responsive to
         weight change in individuals [6], suggesting that modulating the gut microbiome is dynamically
         correlated with the human host’s metabolic phenotype. a b,* a b *































                                                 FMT Introduction
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