Gut Microbiome in Non-Alcoholic Fatty Liver Disease: From Mechanisms to Therapeutic Role

Gupta, Haripriya; Min, Byeong-Hyun; Ganesan, Raja; Gebru, Yoseph Asmelash; Sharma, Satya Priya; Park, Eunju; Won, Sung‐Min; Jeong, Jin‐Ju; Lee, Su-Been; Cha, Min-Gi; Kwon, Goo-Hyun; Jeong, Min-Kyo; Hyun, Ji-Ye; Eom, Jung-A; Park, Heejin; Yoon, Sang Jun; Choi, Miran; Kim, Dong Joon; Suk, Ki Tae

doi:10.3390/biomedicines10030550

Cited by 29 publications

(22 citation statements)

References 188 publications

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“…There are more than 100 trillion microorganisms in the human gut (about 1.5 kg total weight), making it one of the most diverse ecosystems ( 48 ). It has been reported that camel milk can regulate the intestinal flora structure of mice with colitis, reduce the inflammatory response in mice, and reduce colitis in mice ( 49 ).…”

Section: Discussionmentioning

confidence: 99%

Modulatory effect of camel milk on intestinal microbiota of mice with non-alcoholic fatty liver disease

Hao

Liang

et al. 2022

Front. Nutr.

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Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disease of life, usually caused by unhealthy diet and lifestyle. Compared to normal individuals, the structure of the intestinal flora of NAFLD patients is altered accordingly. This study investigates the effect of camel milk on the regulation of intestinal flora structure in mice with high-fat diet-induced NAFLD. NAFLD model was established by feeding C57BL/6J mice a high-fat diet for 12 weeks, meanwhile camel milk (3.0 g/kg/d), cow milk (3.0 g/kg/d), and silymarin (200 mg/kg/d) were administered by gavage, respectively. Food intake and changes of physiological indexes in mice were observed and recorded. The 16S rRNA gene V3-V4 region was sequenced and the intestinal flora diversity and gene function were predicted in the colon contents of mice from different group. The results showed that camel milk enhanced glucolipid metabolism by downregulate the levels of blood glucose and triglyceride (TG) in serum, reduced lipid accumulation by downregulate the level of TG in the liver and improved liver tissue structure in NAFLD mice (p < 0.05). Meanwhile, camel milk had a positive modulatory effect on the intestinal flora of NAFLD mice, increasing the relative abundance of beneficial bacteria and decreasing the relative abundance of harmful bacteria in the intestinal flora of NAFLD mice, and silymarin had a similar modulatory effect. At the genus level, camel milk increased the relative abundance of Bacteroides, norank_f_Muribaculaceae and Alloprevotella and decreased the relative abundance of Dubosiella and Coriobacteriaceae_UCG-002 (p < 0.05). Camel milk also enhanced Carbohydrate metabolism, Amino acid metabolism, Energy metabolism, Metabolism of cofactors and vitamins and Lipid metabolism in NAFLD mice, thus reducing the degree of hepatic lipid accumulation in NAFLD mice and maintaining the normal structure of the liver. In conclusion, camel milk can improve the structure and diversity of intestinal flora and enhance the levels of substance and energy metabolism in NAFLD mice, which has a positive effect on alleviating NAFLD and improving the structure of intestinal flora.

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Section: Discussionmentioning

confidence: 99%

Modulatory effect of camel milk on intestinal microbiota of mice with non-alcoholic fatty liver disease

Hao

Liang

et al. 2022

Front. Nutr.

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“…While there are a variety of microbiome signatures implicated in NAFLD/NASH, the data are relatively immature, and firm conclusions are necessarily difficult due to potential heterogeneity in studied population ages, geographies, and diets, as well as the actual tools used to sequence the microbiome [ 114 ]. Different microbiotal signatures may predispose to NAFLD and liver fibrosis through multiple different pathways which are beyond the scope of this review, though are well-described in Aron-Wisnewsky et al [ 114 ] and Gupta et al [ 115 ]. However, one microbiotal constituent consistently implicated is lipopolysaccharide (LPS), a Gram-negative bacteria cell wall component, which has been recently linked to multiple metabolic diseases including atherosclerosis and T2DM as well as NAFLD [ 113 , 116 ].…”

Section: Bodymentioning

confidence: 99%

Understanding NAFLD: From Case Identification to Interventions, Outcomes, and Future Perspectives

et al. 2023

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While non-alcoholic fatty liver disease (NAFLD) is a prevalent and frequent cause of liver-related morbidity and mortality, it is also strongly associated with cardiovascular disease-related morbidity and mortality, likely driven by its associations with insulin resistance and other manifestations of metabolic dysregulation. However, few satisfactory pharmacological treatments are available for NAFLD due in part to its complex pathophysiology, and challenges remain in stratifying individual patient’s risk for liver and cardiovascular disease related outcomes. In this review, we describe the development and progression of NAFLD, including its pathophysiology and outcomes. We also describe different tools for identifying patients with NAFLD who are most at risk of liver-related and cardiovascular-related complications, as well as current and emerging treatment options, and future directions for research.

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“…In the last decades, fecal transplantation experiments in mice have provided a growing body of evidence about a causal role between GM alterations and NAFLD/NASH development [ 71 , 72 ]. GM was studied in various animal models of NAFLD, and its alteration was found to be associated with NAFLD genesis and progression.…”

Section: Gut Microbiota and Nafld Development In Animal Modelsmentioning

confidence: 99%

“…Several hypotheses have been formulated as to how the GM may contribute to NAFLD development and progression into NASH. As previously mentioned, they include increased intestinal permeability, leading to an increased absorption by the host of microbially produced toxins and metabolites, such as LPS, trimethylamine N-oxide (TMAO), choline, and ethanol, which trigger inflammation and affect immunity [ 71 ]. Infiltrating immune cells such as monocyte-derived macrophages and neutrophil granulocytes, two mediators of the hepatic inflammation during NASH, seem to have a relevant role in the microbiota-mediated worsening of NAFLD; in fact, chemokine receptor antagonists, by inhibiting monocyte recruitment, reduce hepatocyte ballooning, fibrosis, and inflammation in both the Western diet and the MCD diet models [ 87 ].…”

Section: Gut Microbiota and Nafld Development In Animal Modelsmentioning

confidence: 99%

Age-Related NAFLD: The Use of Probiotics as a Supportive Therapeutic Intervention

Campagnoli

Marchesi

Vairetti

et al. 2022

Cells

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Human aging, a natural process characterized by structural and physiological changes, leads to alterations of homeostatic mechanisms, decline of biological functions, and subsequently, the organism becomes vulnerable to external stress or damage. In fact, the elderly population is prone to develop diseases due to deterioration of physiological and biological systems. With aging, the production of reactive oxygen species (ROS) increases, and this causes lipid, protein, and DNA damage, leading to cellular dysfunction and altered cellular processes. Indeed, oxidative stress plays a key role in the pathogenesis of several chronic disorders, including hepatic diseases, such as non-alcoholic fatty liver disease (NAFLD). NAFLD, the most common liver disorder in the Western world, is characterized by intrahepatic lipid accumulation; is highly prevalent in the aging population; and is closely associated with obesity, insulin resistance, hypertension, and dyslipidemia. Among the risk factors involved in the pathogenesis of NAFLD, the dysbiotic gut microbiota plays an essential role, leading to low-grade chronic inflammation, oxidative stress, and production of various toxic metabolites. The intestinal microbiota is a dynamic ecosystem of microbes involved in the maintenance of physiological homeostasis; the alteration of its composition and function, during aging, is implicated in different liver diseases. Therefore, gut microbiota restoration might be a complementary approach for treating NAFLD. The administration of probiotics, which can relieve oxidative stress and elicit several anti-aging properties, could be a strategy to modify the composition and restore a healthy gut microbiota. Indeed, probiotics could represent a valid supplement to prevent and/or help treating some diseases, such as NAFLD, thus improving the already available pharmacological intervention. Moreover, in aging, intervention of prebiotics and fecal microbiota transplantation, as well as probiotics, will provide novel therapeutic approaches. However, the relevant research is limited, and several scientific research works need to be done in the near future to confirm their efficacy.

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Gut Microbiome in Non-Alcoholic Fatty Liver Disease: From Mechanisms to Therapeutic Role

Cited by 29 publications

References 188 publications

Modulatory effect of camel milk on intestinal microbiota of mice with non-alcoholic fatty liver disease

Modulatory effect of camel milk on intestinal microbiota of mice with non-alcoholic fatty liver disease

Understanding NAFLD: From Case Identification to Interventions, Outcomes, and Future Perspectives

Age-Related NAFLD: The Use of Probiotics as a Supportive Therapeutic Intervention

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