Prenatal exposure to diesel exhaust PM2.5 programmed non-alcoholic fatty liver disease differently in adult male offspring of mice fed normal chow and a high-fat diet

Wang, Xiaoke; Yang, Yuxue; Zhu, Piaoyu; Wu, Yifan; Yang, Jing; Yu, Shali; Wei, Haiyan; Qian, Muzhou; Cao, Weiming; Xu, Shenya; Liu, Yingqi; Chen, Gang; Zhao, Xinyuan

doi:10.1016/j.envpol.2019.113366

Cited by 22 publications

(9 citation statements)

References 37 publications

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“…NAFLD develops because of the interaction of genes (epistasis) and environmental factors (exposome) [ 74 , 75 ]. The environmental factors act through intestinal, microbial, and dietary modifications [ 11 , 76 ], and can be linked with exposure to food contaminants, contaminated consumer products or air pollution [ 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 ].…”

Section: Beyond Nafld: the Gut Liver-axis The Gut Barrier And Thmentioning

confidence: 99%

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Ciaula

Baj

Garruti

et al. 2020

JCM

117

112

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The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide and parallels comorbidities such as obesity, metabolic syndrome, dyslipidemia, and diabetes. Recent studies describe the presence of NAFLD in non-obese individuals, with mechanisms partially independent from excessive caloric intake. Increasing evidences, in particular, point towards a close interaction between dietary and environmental factors (including food contaminants), gut, blood flow, and liver metabolism, with pathways involving intestinal permeability, the composition of gut microbiota, bacterial products, immunity, local, and systemic inflammation. These factors play a critical role in the maintenance of intestinal, liver, and metabolic homeostasis. An anomalous or imbalanced gut microbial composition may favor an increased intestinal permeability, predisposing to portal translocation of microorganisms, microbial products, and cell wall components. These components form microbial-associated molecular patterns (MAMPs) or pathogen-associated molecular patterns (PAMPs), with potentials to interact in the intestine lamina propria enriched in immune cells, and in the liver at the level of the immune cells, i.e., Kupffer cells and stellate cells. The resulting inflammatory environment ultimately leads to liver fibrosis with potentials to progression towards necrotic and fibrotic changes, cirrhosis. and hepatocellular carcinoma. By contrast, measures able to modulate the composition of gut microbiota and to preserve gut vascular barrier might prevent or reverse NAFLD.

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Section: Beyond Nafld: the Gut Liver-axis The Gut Barrier And Thmentioning

confidence: 99%

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Ciaula

Baj

Garruti

et al. 2020

JCM

117

112

View full text Add to dashboard Cite

show abstract

“…Lifestyles which include quality of diet, sedentary life, sweetened beverages, hypercaloric intake, induce potent gut, microbial, and dietary modifications [ 3 , 361 ]. Additional factors playing a key role are food contaminants, contaminated consumer products, or air pollution [ 362 , 363 , 364 , 365 , 366 , 367 , 368 , 369 ]. Diet is a main contributor to gut microbiota diversity and accounts for more than 55% of the variations, compared to about 12% estimated for genetic variation [ 370 ].…”

Section: The Intestinal Barrier: General Implications In Obesity and ...mentioning

confidence: 99%

Intestinal Barrier and Permeability in Health, Obesity and NAFLD

et al. 2021

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The largest surface of the human body exposed to the external environment is the gut. At this level, the intestinal barrier includes luminal microbes, the mucin layer, gastrointestinal motility and secretion, enterocytes, immune cells, gut vascular barrier, and liver barrier. A healthy intestinal barrier is characterized by the selective permeability of nutrients, metabolites, water, and bacterial products, and processes are governed by cellular, neural, immune, and hormonal factors. Disrupted gut permeability (leaky gut syndrome) can represent a predisposing or aggravating condition in obesity and the metabolically associated liver steatosis (nonalcoholic fatty liver disease, NAFLD). In what follows, we describe the morphological-functional features of the intestinal barrier, the role of major modifiers of the intestinal barrier, and discuss the recent evidence pointing to the key role of intestinal permeability in obesity/NAFLD.

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“…More recently, another study in 2019 discovered that prenatal and postnatal (4 weeks) PM 2.5 exposure increased lipogenesis and worsened fatty acid oxidation differentially in mice consuming chow and high-fat diet [67]. Moreover, another study using continued PM exposure throughout development in mice showed transcriptomic changes in the liver in adulthood [68].…”

Section: Risk Of Future Respiratory and Metabolic Disordersmentioning

confidence: 99%

Particulate Matter, an Intrauterine Toxin Affecting Foetal Development and Beyond

et al. 2021

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Air pollution is the 9th cause of the overall disease burden globally. The solid component in the polluted air, particulate matters (PMs) with a diameter of 2.5 μm or smaller (PM2.5) possess a significant health risk to several organ systems. PM2.5 has also been shown to cross the blood–placental barrier and circulate in foetal blood. Therefore, it is considered an intrauterine environmental toxin. Exposure to PM2.5 during the perinatal period, when the foetus is particularly susceptible to developmental defects, has been shown to reduce birth weight and cause preterm birth, with an increase in adult disease susceptibility in the offspring. However, few studies have thoroughly studied the health outcome of foetuses due to intrauterine exposure and the underlying mechanisms. This perspective summarises currently available evidence, which suggests that intrauterine exposure to PM2.5 promotes oxidative stress and inflammation in a similar manner as occurs in response to direct PM exposure. Oxidative stress and inflammation are likely to be the common mechanisms underlying the dysfunction of multiple systems, offering potential targets for preventative strategies in pregnant mothers for an optimal foetal outcome.

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Prenatal exposure to diesel exhaust PM2.5 programmed non-alcoholic fatty liver disease differently in adult male offspring of mice fed normal chow and a high-fat diet

Cited by 22 publications

References 37 publications

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

Intestinal Barrier and Permeability in Health, Obesity and NAFLD

Particulate Matter, an Intrauterine Toxin Affecting Foetal Development and Beyond

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