Heavy metals play an important endocrine-disrupting role in the health consequences. However, the endocrine-disrupting mechanism of heavy metals is unclear. There are long-term and low-level metal/element exposure scenes for the human body in real life. Therefore, animal models exposed to high doses of heavy metals may not provide key information to elucidate the underlying pathogeny of human diseases. This review collects current knowledge regarding the endocrine-disrupting roles of heavy metals such as lead (Pb), cadmium (Cd), arsenic (As), mercury (Hg), nickel (Ni), copper (Cu), zinc (Zn), and manganese (Mn), summarizes the possible molecular mechanisms of these endocrine-disrupting chemicals (EDCs), and briefly evaluates their endocrine toxicity on animals and humans.

Cardiovascular diseases are the principal cause of death worldwide. The potentially serious adverse effects of therapeutic drugs lead to growing awareness of the role of Chinese herbal medicine in the treatment of cardiovascular diseases. Chinese herbal medicine has been widely used in many countries especially in China from antiquity, however, the mechanisms by which herbal medicine acts in the prevention and treatment of cardiovascular diseases are far from clear. In this review, we briefly describe the characteristics of Chinese herbal medicine by comparing with western medicine. Then we summarize the formulae and herbs/natural products applied in the clinic and animal studies being sorted according to the specific cardiovascular diseases. Most importantly, we elaborate the existing investigations into mechanisms by which herbal compounds act at the cellular levels, including vascular smooth muscle cells, endothelial cells, cardiomyocytes and immune cells. Future research should focus on well-designed clinic trial, in-depth mechanic study, investigations on side effects of herbs and drug interactions. Studies on developing new agents with effectiveness and safety from traditional Chinese medicine is promising for prevention and treatment of patients with cardiovascular diseases.

Background & aims: Emerging evidence supports ambient fine particulate matter (PM_2.5) exposure is associated with insulin resistance (IR) and hepatic lipid accumulation. In this study, we aimed to evaluate the sex-dependent vulnerability in response to PM_2.5 exposure and investigate the underlying mechanism by which PM_2.5 modulates hepatic lipid metabolism. Methods: Both male and female C57BL/6 mice were randomly assigned to ambient PM_2.5 or filtered air for 24 weeks via a whole body exposure system. High-coverage quantitative lipidomics approaches and liquid chromatography-mass spectrometry techniques were performed to measure hepatic metabolites and hormones in plasma. Metabolic studies, histological analyses, as well as gene expression levels and molecular signal transduction analysis were applied to examine the effects and mechanisms by which PM_2.5 exposure-induced metabolic disorder. Results: Female mice were more susceptible than their male counterparts to ambient PM_2.5 exposure-induced IR and hepatic lipid accumulation. The hepatic lipid profile was changed in response to ambient PM_2.5 exposure. Levels of hepatic triacylglycerols (TAGs), free fatty acids (FFAs) and cholesterol were only increased in female mice from PM group compared to control group. Plasmalogens were dysregulated in the liver from PM_2.5-exposed mice as well. In addition, exposure to PM_2.5 led to enhanced hepatic ApoB and microsomal triglyceride transport protein expression in female mice. Finally, PM_2.5 exposure inhibited hypothalamus-pituitary-adrenal (HPA) axis and decreased glucocorticoids levels, which may contribute to the vulnerability in PM_2.5-induced metabolic dysfunction. Conclusions: Ambient PM_2.5 exposure inhibited HPA axis and demonstrated sex-associated differences in its effects on IR and disorder of hepatic lipid metabolism. These findings provide new mechanistic evidence of hormone regulation in air pollution-mediated metabolic abnormalities of lipids and more personalized care should be considered in terms of sex-specific risk factors.

Microplastics (MPs), the emerging environmental pollutants, have attracted global attention due to the potential public health challenge and ecological security risk. Recent studies suggested liver as a vulnerable organ to MPs exposure, evidenced by abnormal hepatic lipid metabolism upon MPs intake in multiple animal species. However, the specific changes of lipid metabolism in mammalian livers, as well as the underlying mechanisms, remain to be elucidated. In the present study, C57BL/6 mice were randomly assigned to normal drinking water or drinking water containing 100 μg L^-1 or 1000 μg L^-1 polystyrene (PS) MPs for 8 weeks. MPs exposure exerted no significant effect on body weight, serum triglyceride or total cholesteryl esters. However, mice showed impaired glucose tolerance and hepatic lipid deposition in response to high-dose MPs administration. Further lipidomic analysis showed significant alteration in hepatic lipid species particularly with free fatty acids (FFAs) and triacylglycerols (TAGs) in mice exposed to MPs. Meanwhile, the liver transcriptional profile indicated MPs exposure-induced differentially expressed genes (DEGs) were enriched in pathways of lipid metabolism and unfolded protein response. Furthermore, most altered lipid species were significantly correlated with DEGs enriched in lipid metabolic signaling. These findings provide lipidomic and transcriptional signatures of liver in response to MPs exposure, which will shed light on further understanding of the metabolic toxicity of MPs.

Obesity is an escalating public health challenge and contributes tremendously to the disease burden globally. New therapeutic strategies are required to alleviate the health impact of obesity-related metabolic dysfunction. Brown adipose tissue is specialized for dissipating chemical energy for thermogenesis as a defense against cold environment. Intriguingly, the brown-fat like adipocytes that dispersed throughout white adipose tissue in rodents and humans, called “brite” or “beige” adipocytes, share similar thermogenic characteristics to brown adipocytes. Recently, researchers have focused on cognition of these thermogenic adipose tissues. Some factors have been identified to regulate the development and function of thermogenic adipose tissues. Cold exposure, pharmacological conditions and lifestyle can enhance non-shivering thermogenesis and metabolism via some mechanisms. However, environmental pollutants, such as ambient fine particulates and ozone, may impair the function of these thermogenic adipose tissues and thereby induce metabolic dysfunction. In this review, the origin, function and influencing factors of thermogenic adipose tissues were summarized and it will provide insights into identifying new therapeutic strategies for the treatment of obesity and obesity-related diseases.