The global incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) has surged in recent years, potentially impacted by both high-energy food intake (e.g., high-fat diet, HFD) and environmental pollutants like microplastics (MPs). However, the combined impacts of MPs exposure and HFD feeding, particularly under long-time exposure, low concentrations MPs conditions, on the MASLD progression remain to be fully elucidated. In this study, C57BL/6 J male mice were fed either a normal chow diet or HFD with or without low-dose MPs (polystyrene) exposure (25-30 μg/kg body weight /day) for 14 weeks. The adverse health effects associated with MASLD development were evaluated, including intestinal permeability, gut microbiota composition, hepatic lipid metabolism, and the mediating role of the gut-liver axis. Additionally, HFD with or without low-dose MPs exposure was withdrawn to further verify this process. Our data demonstrated that low-dose MPs exposure or HFD feeding significantly increased the gut permeability, oxidative stress, pro-inflammatory response and apoptosis, while concurrently contributing to gut dysbiosis (e.g., reduced levels of Akkermansia) and MASLD development. Furthermore, low-dose MPs exposure exacerbated these effects in combination with HFD feeding, exhibiting a 'double hit' effect. Notably, the impacts of low-dose MPs exposure combined with HFD feeding on MASLD were difficult to reverse after two weeks withdrawing, likely due to the limited recovery potential of intestinal barrier integrity and gut microbiota homeostasis. These finding underscore the importance of avoiding MPs exposure in the pathogenesis of MASLD, particularly under a metabolic disorder conditions, and provide valuable insights for the developing therapeutic strategies to combat MASLD caused by MPs exposure.

Background: Chronic obstructive pulmonary disease (COPD) has emerged as a leading cause of chronic disease morbidity and mortality globally, posing a substantial public health challenge. Perfluoroalkyl substances (PFAS) are synthetic chemicals known for their high stability and durability. Research has examined their potential link to decreased lung function. Physical activity (PA) has been identified as one of the primary modalities of the non-pharmacological treatment of COPD. Methods: To investigate the relationship between PFAS and COPD, and whether physical activity could reduce the risk of COPD caused by PFAS exposure, we used data from the NHANES 2013–2018, a cross-sectional study. Logistic regression analysis was used to examine the associations between PFAS and COPD in adult populations, and their associations in different PA types. Results: We finally included 4857 participants in the analysis, and found that Sm-PFOS (OR: 1.250), PFOA (OR: 1.398) and n-PFOA (OR: 1.354) were closely related to COPD; After stratified by gender, age and smoking, the results showed that Sm-PFOA (OR: 1.312) was related to COPD in female adult, and PFOA (OR: 1.398) and n-PFOA (OR: 1.354) were associated with COPD in male adults; The associations of Sm-PFOS (OR: 1.280), PFOA (OR: 1.481) and n-PFOA (OR: 1.424)with COPD tended to be stronger and more consistent in over 50 years old adults; Sm-PFOS was related to COPD in current smoker (OR: 1.408), and PFOA was related to COPD in former smoker (OR: 1.487); Besides, in moderate-intensity PA group, there were no associations of Sm-PFOS, PFOA and n-PFOA with COPD stratified by gender, age and smoking. Conclusion: PFAS exposure may increase the risk of developing COPD, but regular moderate-intensity physical activity can protect individuals from evolving to the disease. However, longitudinal studies are needed to support these preliminary findings.

Celiac disease exhibits a higher prevalence among patients with coronavirus disease 2019. However, the potential influence of COVID-19 on celiac disease remains uncertain. Considering the significant association between gut microbiota alterations, COVID-19 and celiac disease, the two-step Mendelian randomization method was employed to investigate the genetic causality between COVID-19 and celiac disease, with gut microbiota as the potential mediators. We employed the genome-wide association study to select genetic instrumental variables associated with the exposure. Subsequently, these variables were utilized to evaluate the impact of COVID-19 on the risk of celiac disease and its potential influence on gut microbiota. Employing a two-step Mendelian randomization approach enabled the examination of potential causal relationships, encompassing: 1) the effects of COVID-19 infection, hospitalized COVID-19 and critical COVID-19 on the risk of celiac disease; 2) the influence of gut microbiota on celiac disease; and 3) the mediating impact of the gut microbiota between COVID-19 and the risk of celiac disease. Our findings revealed a significant association between critical COVID-19 and an elevated risk of celiac disease (inverse variance weighted [IVW]: P = 0.035). Furthermore, we observed an inverse correlation between critical COVID-19 and the abundance of Victivallaceae (IVW: P = 0.045). Notably, an increased Victivallaceae abundance exhibits a protective effect against the risk of celiac disease (IVW: P = 0.016). In conclusion, our analysis provides genetic evidence supporting the causal connection between critical COVID-19 and lower Victivallaceae abundance, thereby increasing the risk of celiac disease.

Background. So far, type 2 diabetes (T2D) is considered as an independent risk factor for various cancers, but the underlying mechanism remains unclear. Methods. SLC24A2 was first identified as a key gene strongly associated with fasting plasma glucose (FPG). Then, overlapped differentially expressed genes (DEGs) between T2D verse control and SLC24A2-high verse SLC24A2-low were extracted and imported into weighted correlation network analysis. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and gene set enrichment analysis were used for functional enrichment analysis of DEGs. Least absolute shrinkage and selection operator was utilized to build a T2D prediction model. Timer and - plotters were employed to find the expression and prognosis of SLC24A2 in pan cancer. Results. Interestingly, both DEGs between T2D verse control and SLC24A2-high verse SLC24A2-low enriched in cancer-related pathways. Moreover, a total of 3719 overlapped DEGs were divided into 8 functional modules. Grey module negatively correlated with T2D and FPG and was markedly involved in ribosome biogenesis. Ten SLC24A2-related genes (RRP36, RPF1, GRWD1, FBL, EXOSC5, BCCIP, UTP14A, TWISTNB, TBL3, and SKIV2L) were identified as hub genes, based on which the LASSO model accurately predicts the occurrence of T2D ( ). In addition, SLC24A2 was only expressed in islet β cells and showed abnormal expression in 17 kinds of cancers and significantly correlated with the prognosis of 10 kinds of cancers. Conclusion. Taken together, SLC24A2 may link T2D and cancer by influencing the ribosome function of islet β cells and play different prognostic roles in different cancers.