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Review
. 2019;38(3):81-88.
doi: 10.12938/bmfh.18-032. Epub 2019 May 8.

The role of gut microbiota in non-alcoholic fatty liver disease: pathways of mechanisms

Chyntia Olivia Maurine Jasirwan  1 , Cosmas Rinaldi Adithya Lesmana  1 , Irsan Hasan  1 , Andri Sanityosos Sulaiman  1 , Rino Alvani Gani  1
Affiliations
Review

The role of gut microbiota in non-alcoholic fatty liver disease: pathways of mechanisms

Chyntia Olivia Maurine Jasirwan et al. Biosci Microbiota Food Health. 2019.

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome. Its prevalence increases with increasing rates of obesity, insulin resistance, and diabetes mellitus. The pathogenesis of NAFLD involves many factors, including the gastrointestinal microbiota. However, there is still debate about the impact of gut dysbiosis in the NAFLD disease progression. Therefore, this paper aims to review the relationship between gut microbiota and other risk factors for NAFLD and how gut dysbiosis plays a role in the pathogenesis of NAFLD. Hopefully, this paper can make an appropriate contribution to the development of NAFLD research in the future.

Keywords: NAFLD; dysbiosis; gut microbiota; inflammatory pathway; metabolic pathway.

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Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper.

Figures

Fig. 1.
Fig. 1.
The role of gut microbiota in the pathogenesis of NAFLD. Dysbiosis of gut microbiota leads to low-grade chronic inflammation. The inflammatory condition itself can also be caused by an increment in ethanol production resulting from gut microbiota activity. The inflammatory condition predisposes individuals to development of metabolic syndrome features and NAFLD. Based on metabolic pathway, an increase in SCFAs and alteration of their components give rise to an increase in adipose tissue and liver DNL. Liver DNL is also caused by suppression of FIAF, enhancing LPL activity. Dysbiosis alters the bile acids profile and lowers FXR signaling causing an increase in liver DNL. Choline conversion to methylamine increases, decreasing VLDL synthesis, and this factor predisposes individuals to the development of fatty liver. PAMPs: pathogen-associated molecular patterns; DAMPs: damage-associated molecular patterns; LPS: lipopolysaccharides; FA: fatty acid; TLR: Toll-like receptor; NLRP-3: nucleotide-binding domain and leucine-rich repeat pyrin 3 domain; ECS: endocannabinoid system; SCFAs: short-chain fatty acids; ChREBP: carbohydrate response element binding protein; DNL: de novo lipogenesis; FIAF: fasting-induced adipose factor; LPL: lipoprotein lipase; FXR: farnesoid X receptor; VLDL: very-low-density lipoprotein; NAFLD: nonalcoholic fatty liver disease.
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