TY - JOUR
T1 - Gut microbiota abnormalities, small intestinal bacterial overgrowth, and non-alcoholic fatty liver disease
T2 - An emerging paradigm
AU - Ghoshal, Uday C.
AU - Goel, Amit
AU - Quigley, Eamonn M.M.
N1 - Publisher Copyright:
© 2020, Indian Society of Gastroenterology.
PY - 2020/2/1
Y1 - 2020/2/1
N2 - Evidence accumulates to implicate a role for the gut microbiota in non-alcoholic fatty liver disease (NAFLD)—a disorder that has reached almost epidemic proportions around the globe. For some time a disturbance in the gut microbiome, small intestinal bacterial overgrowth (SIBO), has been described among patients with liver disease, in general, and in the development and progression of NAFLD to nonalcoholic steatohepatitis (NASH), decompensated liver disease and hepatocellular cancer (HCC), in particular. More recently and permitted by the advent of high-throughput sequencing and allied molecular techniques, a much more detailed analysis of gut microbiota in NAFLD and NASH has become possible. In animal models, several mechanisms have been delineated which reveal how gut bacteria and their products could promote steatosis, hepatic inflammation, fibrosis, cirrhosis, and carcinogenesis. For understandable reasons evidence from human studies is less complete, but here again a plausible case is beginning to emerge to incriminate microbiota in NAFLD and NASH pathogenesis. Therapeutic interventions based on the modulation of the microbiome have been explored to some extent, but their application to everyday medical practice is still in the future.
AB - Evidence accumulates to implicate a role for the gut microbiota in non-alcoholic fatty liver disease (NAFLD)—a disorder that has reached almost epidemic proportions around the globe. For some time a disturbance in the gut microbiome, small intestinal bacterial overgrowth (SIBO), has been described among patients with liver disease, in general, and in the development and progression of NAFLD to nonalcoholic steatohepatitis (NASH), decompensated liver disease and hepatocellular cancer (HCC), in particular. More recently and permitted by the advent of high-throughput sequencing and allied molecular techniques, a much more detailed analysis of gut microbiota in NAFLD and NASH has become possible. In animal models, several mechanisms have been delineated which reveal how gut bacteria and their products could promote steatosis, hepatic inflammation, fibrosis, cirrhosis, and carcinogenesis. For understandable reasons evidence from human studies is less complete, but here again a plausible case is beginning to emerge to incriminate microbiota in NAFLD and NASH pathogenesis. Therapeutic interventions based on the modulation of the microbiome have been explored to some extent, but their application to everyday medical practice is still in the future.
KW - Cirrhosis
KW - Dysbiosis
KW - Metabolic syndrome
KW - Microbiota
KW - Nonalcoholic steatohepatitis
KW - Obesity
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U2 - 10.1007/s12664-020-01027-w
DO - 10.1007/s12664-020-01027-w
M3 - Review article
C2 - 32291578
AN - SCOPUS:85083787782
SN - 0254-8860
VL - 39
SP - 9
EP - 21
JO - Indian Journal of Gastroenterology
JF - Indian Journal of Gastroenterology
IS - 1
ER -