Increasing attention has recently been paid to the harm of polycystic ovary syndrome (PCOS) to women. However, due to the inconsistency of global clinical diagnostic standards and the differing allocation of medical resources among different regions, there is a lack of comprehensive estimation of the global incidence and disability-adjusted life years (DALYs) of PCOS. Thus, it is difficult to assess the disease burden. We extracted PCOS disease data from 1990 to 2019 from the Global Burden of Disease Study (GBD) 2019 and estimated the incidence, DALYs, and the corresponding age-standardized rates (ASRs) of PCOS, as well as the socio-demographic index (SDI) quintiles, to describe epidemiological trends at the global level, encompassing 21 regions and 204 countries and territories. Globally, the incidence and DALYs of PCOS have increased. Its ASR also shows an increasing trend. Among them, the high SDI quintile seems relatively stable, whereas other SDI quintiles are constantly rising over time. Our research has provided clues regarding the disease pattern and epidemic trend of PCOS and analyzed the possible causes of disease burden in some specific countries and territories, which may have some value in health resource allocation and health policy formulation and prevention strategies.

Background: As a central organ of energy metabolism, the liver is closely related to selenium for its normal function and disease development. However, the underlying roles of mitochondrial energy metabolism and mitophagy in liver fibrosis associated with selenium remain unclear. Methods: 28 rats were randomly divided into normal, low-selenium, nano-selenium supplement-1, and supplement-2 groups for a 12-week intervention. We observed pathological and ultrastructural changes in the liver and analyzed the effects of selenium deficiency and nano-selenium supplementation on liver metabolic activities and crucial proteins expression of mammalian target of the rapamycin (mTOR) signaling pathway. Results: Selenium deficiency caused liver pathological damage and fibrosis with the occurrence of mitophagy by disrupting normal metabolic activities; meanwhile, the mTOR signaling pathway was up-regulated to enhance mitophagy to clear damaged mitochondria. Furthermore, nano-selenium supplements could reduce the severity of pathological damage and fibrosis in livers and maintain normal energy metabolic activity. With the increased concentrations of nano-selenium supplement, swelling mitochondria and mitophagy gradually decreased, accompanied by the higher expression of mTOR and phosphorylation-modified mTOR proteins and lower expression of unc-51 like autophagy activating kinase 1 (ULK1) and phosphorylation-modified ULK1 proteins. Conclusions: Mitophagy regulated by the mTOR signaling pathway plays a dual protective role on low-selenium inducing liver fibrosis and nano-selenium supplements preventing liver fibrosis. Mitochondrial energy metabolism plays an important role in these processes as well.

As common pathogenic agents in the world and widely distributed globally, T-2 toxin and selenium deficiency might exacerbate toxic effects by combined exposure, posing a dramatic health hazard to humans and animals. In this study, we aim to elucidate the underlying mechanisms of renal fibrosis triggered by T-2 toxin and selenium deficiency exposure. A total of thirty-two rats are randomly divided into the normal control, T-2 toxin, selenium deficiency, and combined intervention groups. T-2 toxin (100 ng/g) is intragastric gavaged to the rats in compliance with the body weight. Both the standard (containing selenium 0.20 mg/Kg) and selenium-deficient (containing selenium 0.02 mg/Kg) diets were manufactured adhering to the AIN-93 formula. After 12 weeks of intervention, renal tissue ultrastructural and pathological changes, inflammatory infiltration, epithelial mesenchymal transition (EMT), and extracellular matrix (ECM) deposition are evaluated, respectively. Metabolomics analysis is conducted to explore the underlying pathology of renal fibrosis, followed by the validation of potential mechanisms at gene and protein levels. T-2 toxin and selenium deficiency exposure results in podocyte foot process elongation or fusion, tubular vacuolization and dilatation, and collagen deposition in the kidneys. Additionally, it also increases inflammatory infiltration, EMT conversion, and ECM deposition. Metabolomics analysis suggests that T-2 toxin and selenium deficiency influence amino acid and cholesterol metabolism, respectively, and the estrogen signaling pathway is probably engaged in renal fibrosis progression. Moreover, T-2 toxin and selenium deficiency are found to regulate the expressions of the ERα/PI3K/Akt signaling pathway. In conclusion, T-2 toxin and selenium deficiency synergistically exacerbate renal fibrosis through regulating the ERα/PI3K/Akt signaling pathway, and inflammatory infiltration, EMT and ECM deposition are involved in this process.

Bone mineral density (BMD) is a key parameter widely used in the assessment of bone health. Although many investigations have explored the relationship between trace elements and BMD, there are fewer studies focused on serum copper and BMD, especially for adolescents. Using data extracted from the National Health and Nutrition Examination Survey, we applied a multiple-linear regression and smooth curve fitting to assess the relationship between serum copper and BMD. A total of 910 participants were finally included in this study. After adjusting for relevant covariates, serum copper was negatively associated with lumbar spine BMD (β = −0.057, 95% CI: −0.109 to −0.005), trunk bone BMD (β = −0.068, 95% CI: −0.110 to −0.026), pelvis BMD (β = −0.085, 95% CI: −0.145 to −0.024), subtotal BMD (β = −0.072, 95% CI: −0.111 to −0.033), and total BMD (β = −0.051, 95% CI: −0.087 to −0.016) (p < 0.05). In quartile analysis, the highest level of serum copper was associated with decreased BMD when compared with those at the lowest quartile (p < 0.05). The stratified analysis revealed a significant interaction between age and the effects of serum copper on trunk bone BMD (p = 0.022) and pelvis BMD (p = 0.018). Meanwhile, the higher level of serum copper was negatively associated with BMD in males, and gender modified the relationship (p < 0.001). Future longitudinal studies will be necessary for a more definitive interpretation of our results.

Osteoarthritis (OA) is a prevalent and disabling joint disorder characterized by progressive cartilage degradation, subchondral bone changes, synovial inflammation, and chronic pain. While traditionally attributed to mechanical and age-related factors, increasing attention has been directed toward the role of nutritional components in disease modulation. This article critically examines the emerging role of three essential trace elements, zinc, copper, and selenium, in the pathophysiology of OA. These micronutrients are fundamental to antioxidant defense, immune modulation, and extracellular matrix (ECM) integrity. Altered systemic or local levels of zinc, copper, and selenium have been associated with oxidative stress, inflammation, and dysregulated cartilage metabolism in OA. Drawing on clinical studies, in vivo and in vitro experimental models, and population-based data, we synthesize evidence on trace element status in OA patients, mechanistic pathways, and therapeutic potential, including emerging nanomedicine strategies that enhance the targeted delivery and therapeutic efficacy of trace elements in joint tissues. This review highlights the need for integrated trace element profiling in OA research and clinical care and supports the exploration of targeted nutritional interventions in OA prevention and management.