Publications by authors named "Wenpu Shao"

Article Synopsis
  • Maternal exposure to particulate matter (PM) may disrupt metabolic processes, particularly glucose and lipid metabolism, in offspring on a high-fat diet (HFD), but the effects could vary by gender.
  • In a study, female mice exposed to PM before and during pregnancy showed that their female offspring developed glucose intolerance and insulin resistance on an HFD, while males did not.
  • Analysis revealed liver issues in female offspring, including altered structure and impaired function, suggesting that prenatal PM exposure negatively impacts their metabolism and highlights the liver's role in these gender-specific effects.
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Background: Previous studies found that urinary phthalates (PAEs) metabolites may be associated with increased serum uric acid concentration and hyperuricemia risk. However, no population-based study has investigated the underlying biological mechanisms.

Methods: This nationwide cross-sectional study analyzed the data from the National Health and Nutrition Examination Survey (NHANES) 2003-2018.

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PM exposure has been found to cause gut dysbiosis and impair glucose homeostasis in human and animals, yet their underlying biological connection remain unclear. In the present study, we aim to investigate the biological significance of gut microbiota in PM-induced glucose metabolic abnormalities. Our results showed that microbiota depletion by antibiotics treatment significantly alleviated PM-induced glucose intolerance and insulin resistance, as indicated by the intraperitoneal glucose tolerance test, glucose-induced insulin secretion, insulin tolerance test, insulin-induced phosphorylation levels of Akt and GSK-3β in insulin sensitive tissues.

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Previous research has indicated that the cholinergic anti-inflammatory pathway (CAP) can regulate the duration and intensity of inflammatory responses. A wide range of research has demonstrated that PM exposure may induce various negative health effects via pulmonary and systemic inflammations. To study the potential role of the CAP in mediating PM-induced effects, mice were treated with vagus nerve electrical stimulation (VNS) to activate the CAP before diesel exhaust PM (DEP) instillation.

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Background: Ambient fine particulate matter (PM) exposure increases local and systemic interleukin-6 (IL-6). However, the pathogenic role of IL-6 signalling following PM exposure, particularly in the development of pulmonary dysfunction and abnormal glucose homeostasis, has hardly been investigated.

Results: In the study, IL-6 receptor (IL-6R)-deficient (IL-6R) and wildtype littermate (IL-6R) mice were exposed to concentrated ambient PM (CAP) or filtered air (FA), and their pulmonary and metabolic responses to these exposures were analyzed.

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Epidemiological and animal studies have shown that maternal fine particulate matters (PM) exposure correlates with various adverse pregnancy outcomes such as low birth weight (LBW) of offspring. However, the underlying biological mechanisms have not been fully understood. In this study, female C57Bl/6 J mice were exposed to filtered air (FA) or concentrated ambient PM (CAP) during pregestational and gestational periods, and metabolomics was performed to analyze the metabolic features in maternal serum and placenta by liquid chromatography-mass spectrometry (LC-MS).

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Ambient fine particulate matter (PM) has a marked temporospatial variation in chemical composition, but how the composition of PM influences its toxicity remains elusive. To explore the roles of individual PM components in the pathogenesis following PM exposure, we prepared water-soluble (WS-DEP) and water-insoluble (WIS-DEP) fractions of diesel exhaust particles (DEP) and performed 15-week intratracheal instillation on C57Bl/6J mice using these fractions. Their effects on pulmonary and systemic inflammation, hepatic steatosis and insulin resistance, systemic glucose homeostasis, and gut microbiota were then assessed.

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