Effects of environmental contaminants in water resources on nonalcoholic fatty liver disease

Zheng, Shuilin; Yang, Yue; Wen, Cong; Liu, Wenya; Cao, Linghui; Feng, Xiangling; Chen, Jihua; Wang, Hui; Tang, Yan; Liu, Tian; Wang, Xiaoyan

doi:10.1016/j.envint.2021.106555

Cited by 57 publications

(35 citation statements)

References 56 publications

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“…Regardless of primary causes, the risk of developing severe fatty liver disease is well-known to be modified by other factors both genetic and lifestyle 45 , 52 , 122 . In contrast to the other liver diseases discussed in this review, there are several lines of evidence that indicate that environmental toxicants may be a risk factor for the development and progression of fatty liver diseases, especially due to obesity/insulin resistance 46 , 47 , 48 , 49 , 123 , 124 , 125 . There are relatively strong data linking exposure to persistent organic pollutants ( e.g ., dioxin), volatile organic compounds ( e.g ., vinyl chloride; VC), metals ( e.g ., arsenic) as well as some herbicides/fungicides with the development of experimental and human fatty liver disease 46 , 124 .…”

Section: Fatty Liver Diseases (Ald Nafld/mafld Tafld)mentioning

confidence: 91%

“…This famous quote by the astrophysicist Neil deGrasse Tyson highlights the difficulty in making conclusions on what is known when all data are not available. This review will highlight the knowledgebase of environmental exposure as a potential risk-modifying agent for the development of liver disease by other causes ( Table 1 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 ). We will focus on what is known, as well as prospects for better understanding ( i.e ., unknowns).…”

Section: Introductionmentioning

confidence: 99%

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Environmental exposure as a risk-modifying factor in liver diseases: Knowns and unknowns

Beier

Arteel²

2021

Acta Pharmaceutica Sinica B

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Liver diseases are considered to predominantly possess an inherited or xenobiotic etiology. However, inheritance drives the ability to appropriately adapt to environmental stressors, and disease is the culmination of a maladaptive response. Thus “pure” genetic and “pure” xenobiotic liver diseases are modified by each other and other factors, identified or unknown. The purpose of this review is to highlight the knowledgebase of environmental exposure as a potential risk modifying agent for the development of liver disease by other causes. This exercise is not to argue that all liver diseases have an environmental component, but to challenge the assumption that the current state of our knowledge is sufficient in all cases to conclusively dismiss this as a possibility. This review also discusses key new tools and approaches that will likely be critical to address this question in the future. Taken together, identifying the key gaps in our understanding is critical for the field to move forward, or at the very least to “know what we don't know.”

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Section: Fatty Liver Diseases (Ald Nafld/mafld Tafld)mentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Environmental exposure as a risk-modifying factor in liver diseases: Knowns and unknowns

Beier

Arteel²

2021

Acta Pharmaceutica Sinica B

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“…Emerging evidence also suggests that environmental contaminants may play an underappreciated role in gut dysbiosis and NAFLD development [4][5][6][7][8][9][10][11]. Specifically, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental organochloride pollutant, induces steatosis and the progression to steatohepatitis with fibrosis in mice resembling human NAFLD development [9,[12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Aryl Hydrocarbon Receptor (AhR) Activation by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) Dose-Dependently Shifts the Gut Microbiome Consistent with the Progression of Non-Alcoholic Fatty Liver Disease

Fling

Zacharewski

2021

IJMS

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Gut dysbiosis with disrupted enterohepatic bile acid metabolism is commonly associated with non-alcoholic fatty liver disease (NAFLD) and recapitulated in a NAFLD-phenotype elicited by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice. TCDD induces hepatic fat accumulation and increases levels of secondary bile acids, including taurolithocholic acid and deoxycholic acid (microbial modified bile acids involved in host bile acid regulation signaling pathways). To investigate the effects of TCDD on the gut microbiota, the cecum contents of male C57BL/6 mice orally gavaged with sesame oil vehicle or 0.3, 3, or 30 µg/kg TCDD were examined using shotgun metagenomic sequencing. Taxonomic analysis identified dose-dependent increases in Lactobacillus species (i.e., Lactobacillus reuteri). Increased species were also associated with dose-dependent increases in bile salt hydrolase sequences, responsible for deconjugation reactions in secondary bile acid metabolism. Increased L. reuteri levels were further associated with mevalonate-dependent isopentenyl diphosphate (IPP) biosynthesis and o-succinylbenzoate synthase, a menaquinone biosynthesis associated gene. Analysis of the gut microbiomes from cirrhosis patients identified an increased abundance of genes from the mevalonate-dependent IPP biosynthesis as well as several other menaquinone biosynthesis genes, including o-succinylbenzoate synthase. These results extend the association of lactobacilli with the AhR/intestinal axis in NAFLD progression and highlight the similarities between TCDD-elicited phenotypes in mice to human NAFLD.

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“…Environmental factors include sedentary life-style, a high-calorific and/or high-fat diet, especially rich in saturated fats [ 13 ], as well as environmental pollutants such as heavy metals, chlorination by-products, microcystins etc. [ 14 ]. In addition, various hepatotoxic-drugs such as valproic acid, aspirin, amiodarone and ibuprofen are also known to cause NAFLD by impairing lipid metabolism [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Exploring the Gamut of Receptor Tyrosine Kinases for Their Promise in the Management of Non-Alcoholic Fatty Liver Disease

Bhave

2021

Biomedicines

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Recently, non-alcoholic fatty liver disease (NAFLD) has emerged as a predominant health concern affecting approximately a quarter of the world’s population. NAFLD is a spectrum of liver ailments arising from nascent lipid accumulation and leading to inflammation, fibrosis or even carcinogenesis. Despite its prevalence and severity, no targeted pharmacological intervention is approved to date. Thus, it is imperative to identify suitable drug targets critical to the development and progression of NAFLD. In this quest, a ray of hope is nestled within a group of proteins, receptor tyrosine kinases (RTKs), as targets to contain or even reverse NAFLD. RTKs control numerous vital biological processes and their selective expression and activity in specific diseases have rendered them useful as drug targets. In this review, we discuss the recent advancements in characterizing the role of RTKs in NAFLD progression and qualify their suitability as pharmacological targets. Available data suggests inhibition of Epidermal Growth Factor Receptor, AXL, Fibroblast Growth Factor Receptor 4 and Vascular Endothelial Growth Factor Receptor, and activation of cellular mesenchymal-epithelial transition factor and Fibroblast Growth Factor Receptor 1 could pave the way for novel NAFLD therapeutics. Thus, it is important to characterize these RTKs for target validation and proof-of-concept through clinical trials.

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Effects of environmental contaminants in water resources on nonalcoholic fatty liver disease

Cited by 57 publications

References 56 publications

Environmental exposure as a risk-modifying factor in liver diseases: Knowns and unknowns

Environmental exposure as a risk-modifying factor in liver diseases: Knowns and unknowns

Aryl Hydrocarbon Receptor (AhR) Activation by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) Dose-Dependently Shifts the Gut Microbiome Consistent with the Progression of Non-Alcoholic Fatty Liver Disease

Exploring the Gamut of Receptor Tyrosine Kinases for Their Promise in the Management of Non-Alcoholic Fatty Liver Disease

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