scholarly journals Potential role of gut microbiota, the proto-oncogene PIKE (Agap2) and cytochrome P450 CYP2W1 in promotion of liver cancer by alcoholic and nonalcoholic fatty liver disease and protection by dietary soy protein

2020 ◽  
Vol 325 ◽  
pp. 109131 ◽  
Author(s):  
Martin J. Ronis ◽  
Kelly E. Mercer ◽  
Kartik Shankar ◽  
Casey Pulliam ◽  
Kim Pedersen ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Caihua Wang ◽  
Chunpeng Zhu ◽  
Liming Shao ◽  
Jun Ye ◽  
Yimin Shen ◽  
...  

Nonalcoholic fatty liver disease (NAFLD) is a major health threat around the world and is characterized by dysbiosis. Primary bile acids are synthesized in the liver and converted into secondary bile acids by gut microbiota. Recent studies support the role of bile acids in modulating dysbiosis and NAFLD, while the mechanisms are not well elucidated. Dysbiosis may alter the size and the composition of the bile acid pool, resulting in reduced signaling of bile acid receptors such as farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5). These receptors are essential in lipid and glucose metabolism, and impaired bile acid signaling may cause NAFLD. Bile acids also reciprocally regulate the gut microbiota directly via antibacterial activity and indirectly via FXR. Therefore, bile acid signaling is closely linked to dysbiosis and NAFLD. During the past decade, stimulation of bile acid receptors with their agonists has been extensively explored for the treatment of NAFLD in both animal models and clinical trials. Early evidence has suggested the potential of bile acid receptor agonists in NAFLD management, but their long-term safety and effectiveness need further clarification.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2642 ◽  
Author(s):  
Marica Meroni ◽  
Miriam Longo ◽  
Paola Dongiovanni

Nonalcoholic fatty liver disease (NAFLD) encompasses a broad spectrum of pathological hepatic conditions ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), which may predispose to liver cirrhosis and hepatocellular carcinoma (HCC). Due to the epidemic obesity, NAFLD is representing a global health issue and the leading cause of liver damage worldwide. The pathogenesis of NAFLD is closely related to insulin resistance (IR), adiposity and physical inactivity as well as genetic and epigenetic factors corroborate to the development and progression of hepatic steatosis and liver injury. Emerging evidence has outlined the implication of gut microbiota and gut-derived endotoxins as actively contributors to NAFLD pathophysiology probably due to the tight anatomo-functional crosstalk between the gut and the liver. Obesity, nutrition and environmental factors might alter intestinal permeability producing a favorable micro-environment for bacterial overgrowth, mucosal inflammation and translocation of both invasive pathogens and harmful byproducts, which, in turn, influence hepatic fat composition and exacerbated pro-inflammatory and fibrotic processes. To date, no therapeutic interventions are available for NAFLD prevention and management, except for modifications in lifestyle, diet and physical exercise even though they show discouraging results due to the poor compliance of patients. The premise of this review is to discuss the role of gut–liver axis in NAFLD and emphasize the beneficial effects of probiotics on gut microbiota composition as a novel attractive therapeutic strategy to introduce in clinical practice.


2012 ◽  
Vol 107 (12) ◽  
pp. 1932 ◽  
Author(s):  
Lucia Malaguarnera ◽  
Michelino D Rosa ◽  
Anna M Zambito ◽  
Nicola dellʼOmbra ◽  
Robert D Marco ◽  
...  

2017 ◽  
Vol 58 (7) ◽  
pp. 1399-1416 ◽  
Author(s):  
Aafke W. F. Janssen ◽  
Tom Houben ◽  
Saeed Katiraei ◽  
Wieneke Dijk ◽  
Lily Boutens ◽  
...  

2017 ◽  
Vol 3 (3) ◽  
pp. 165-168 ◽  
Author(s):  
Yong Jiang ◽  
Tao Han ◽  
Zhi-Guang Zhang ◽  
Man Li ◽  
Feng-Xiang Qi ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Melisa Kozaczek ◽  
Walter Bottje ◽  
Diyana Albataineh ◽  
Reza Hakkak

Obesity can lead to chronic health complications such as nonalcoholic fatty liver disease (NAFLD). NAFLD is characterized by lipid aggregation in the hepatocytes and inflammation of the liver tissue as a consequence that can contribute to the development of cirrhosis and hepatocellular carcinoma (HCC). Previously, we reported that feeding obese Zucker rats with soy protein isolate (SPI) can reduce liver steatosis when compared with a casein (CAS) diet as a control. However, the effects of SPI on cytochrome P450 (CYP) in an obese rat model are less known. In addition, there is a lack of information concerning the consumption of soy protein in adolescents and its effect in reducing the early onset of NAFLD in this group. Our main goal was to understand if the SPI diet had any impact on the hepatic CYP gene expression when compared with the CAS diet. For this purpose, we used the transcriptomic data obtained in a previous study in which liver samples were collected from obese rats after short-term (eight-week) and long-term (16-week) feeding of SPI (n = 8 per group). To analyze this RNAseq data, we used Ingenuity Pathway Analysis (IPA) software. Comparing short- vs long-term feeding revealed an increase in the number of downregulated CYP genes from three at 8 weeks of SPI diet to five at 16 weeks of the same diet (P ≤ 0.05). On the other hand, upregulated CYP gene numbers showed a small increase in the long-term SPI diet compared to the short-term SPI diet, from 14 genes at 8 weeks to 17 genes at 16 weeks (P ≤ 0.05). The observed changes may have an important role in the attenuation of liver steatosis.


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