Page 8 - Introduction to FMT

FMT Introduction

Leaky gut or loss of intestinal integrity may facilitate the development of cardiometabolic disorders due
to alterations in composition and diversity of gut microbiota. A close association of microbial translocation
with the risk of cardiovascular disease (CVD) have recently been established[62,63], with probiotic
bacteria having raised plasma unconjugated bile acid concentrations through modulation of the
enterohepatic circulation[64]. It also concomitantly reduced the lipid uptake from the intestine and the
plasma cholesterol level, an indirect risk marker of CVD, by means of regulation of a series of

Extra-intestinal disorders Ref. Publication year Study type

Chronic fatigue syndrome Borody et al[84] 2012 Cohort study

Autoimmune disorders

ITP Borody et al[85] 2011 Case report

Arthritis Scher et al[88] 2013 Observational study

Abdollahi-Roodsaz et al[86] 2014 Experimental study

5/10/2018 Fecal microbiota transplantation broadening its application beyond intestinal disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284325/ 6/16 signaling molecules, such as Farnesoid
X receptor-α and G-protein-coupled receptors[64]. One study illustrated the negative impact of
trimethylamine-N-oxide, an atherogenic compound produced by intestinal flora from choline and
betaine[65,66], on the morbidity and mortality of cardiovascular events[67]. A variety of data have clearly
demonstrated that the intestinal microbiota act as an independent risk factor for CVD, as well as
representing a promising therapeutic target for this disease.

An increasing body of published evidence has recently been generated that demonstrates that
demonstrates the gut microbiota act as an epigenetic factor driving the progression of non-alcoholic
fatty liver disease (NAFLD)[68-70], a metabolic syndrome that manifests in the liver[71]. Intestinal
dysbiosis promotes hepatic injury and inflammation through either a breakdown of the intestinal barrier or
translocation of microbial products[72]. Abundant studies using GF mice models have illustrated that
these special organisms are resistant to steatosis and diet-induced obesity[73]. Le Roy et al[68]
performed an animal study to clarify the role of gut microbiota in the development of NAFLD. They
divided the conventional mice into two groups (responder and non-responder) according to their
response to a high-fat diet (HFD), and found that GF mice receiving FMT from different donors (responder
and non-responder) developed comparable results on the HFD. The GF group that received microbiota
from the responder group developed steatosis and harbored a larger number of Barnesiella and
Roseburia, whereas Allobaculum was higher in the other group[68]. Further evidence has proved that
intestinal permeability increased and endotoxemia developed in NAFLD patients. This indicates that
microbiota-targeting therapy might be useful in treating NAFLD and obesity.

FMT Introduction