Aims/Introduction: Iron metabolism can directly or indirectly affect the occurrence and development of type 2 diabetes. This meta-analysis and systematic review aimed to analyze the association between serum iron metabolism indicators and type 2 diabetes. Materials and Methods: The databases PubMed and Embase were searched for studies on the correlations between serum iron metabolism indicators (iron, ferritin, transferrin, hepcidin and soluble transferrin receptor) and type 2 diabetes since January 2006. Relevant data were extracted from the included studies, and meta-analysis was carried out. Results: A total of 12 case-control and cohort studies were analyzed. Of the 12 studies, 11 described the correlation between serum ferritin levels and type 2 diabetes. The median and high serum ferritin concentrations were significantly associated with the risks of type 2 diabetes (odds ratio [OR] 1.20, 95% confidence interval [CI] 1.08-1.33 and OR 1.43, 95% CI 1.29-1.59, respectively). However, the low concentration was not correlated with the risk of type 2 diabetes (OR 0.99, 95% CI 0.89-1.11). No significant association was observed between serum soluble transferrin receptor and type 2 diabetes, whereas the soluble transferrin receptor-to-ferritin ratio was significantly inversely related to the risk of type 2 diabetes in the median and high ratio subgroups (OR 0.71, 95% CI 0.51, 0.99 and OR 0.65, 95% CI 0.45-0.95). Conclusions: The elevated serum ferritin was one of the risk factors for type 2 diabetes, and soluble transferrin receptor-to-ferritin ratio was inversely related to the risk of type 2 diabetes. A systematic review showed that serum transferrin and hepcidin might be directly or indirectly related to the development of diabetes.

Background: To assess the effect of obesity or a high body mass index (BMI) on the risk of severe outcomes in patients with coronavirus disease 2019 (COVID-19). Methods: Studies on the relationship between BMI or obesity and COVID-19 since December 2019. The odds ratio (OR) and weighted mean difference (WMD) with their 95% confidence intervals (CIs) were used to assess the effect size. Results: BMI was significantly increased in COVID-19 patients with severe illness (WMD: 1.18; 95% CI: 0.42–1.93), who were admitted to an intensive care unit (ICU) (WMD: 1.46; 95% CI: 0.96–1.97), who required invasive mechanical ventilation (IMV) (WMD: 2.70, 95% CI: 1.05–4.35) and who died (WMD: 0.91, 95% CI: 0.02–1.80). In Western countries, obesity (BMI of ≥30 kg/m 2 ) increased the risk of hospitalization (OR: 2.08; 95% CI: 1.22–3.54), admission to an ICU (OR: 1.54; 95% CI: 1.29–1.84), need for IMV (OR: 1.73, 95% CI: 1.38–2.17), and mortality (OR: 1.43; 95% CI: 1.17–1.74) of patients with COVID-19. In the Asian population, obesity (BMI of ≥28 kg/m 2 ) increased the risk of severe illness (OR: 3.14; 95% CI: 1.83–5.38). Compared with patients with COVID-19 and a BMI of <25 kg/m 2 , those with a BMI of 25–30 kg/m 2 and ≥30 kg/m 2 had a higher risk of need for IMV (OR: 2.19, 95% CI: 1.30–3.69 and OR: 3.04; 95% CI: 1.76–5.28, respectively). The risk of ICU admission in patients with COVID-19 and a BMI of ≥30 kg/m 2 was significantly higher than in those with a BMI of 25–30 kg/m 2 (OR: 1.49; 95% CI: 1.00–2.21). Conclusion: As BMI increased, the risks of hospitalization, ICU admission, and need for IMV increased, especially in COVID-19 patients with obesity. Ethics and dissemination: This systematic review and meta-analysis does not require an ethics approval as it does not collect any primary data from patients.

Background: S100 calcium-binding protein A16 (S100A16) is closely related to the onset and progression of tumors. Material/Methods: In the research, the mainly purpose was to investigate the effect of S100A16 on the proliferation ability, invasion, and angiogenesis of HeLa cells. An adenoviral vector overexpressing S100A16 (Ad-S100A16) was constructed and transfected into HeLa cells, forming a stable cells line of overexpression. The effect of S100A16 on the proliferative capacity of HeLa cells was evaluated by a Cell Counting Kit-8 (CCK-8) assay. Cell migration capacity was determined by a Transwell migration assay. Changes in matrix metalloproteinase-2 (MMP-2), MMP-9, E-cadherin, and vimentin expression were evaluated by a cell-based immunofluorescence assay. The effect of S100A16 on angiogenesis was verified by knockout experiment. Results: Overexpression of S100A16 significantly enhanced the proliferative and migratory capacities of HeLa cells (P<0.05), upregulated expression of matrix MMP-2, MMP-9, vimentin, phosphatidylinositol 3 kinase, and phosphorylated protein kinase B, and downregulated expression of E-cadherin. Vascular endothelial growth factor expression increased, phosphatase and tensin homolog expression decreased, and angiogenesis was positively correlated with S100A16 expression. These effects were largely mediated by the activation of the phosphatidylinositol 3 kinase/protein kinase B pathways. Conclusions: S100A16 could promote the proliferation, migration, and tumor angiogenesis of HeLa cells by regulating the phosphatidylinositol 3 kinase/protein kinase B signaling pathways.

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Background During fertility treatment, diminished ovarian reserve (DOR) is a challenge that can seriously affect a patient’s reproductive potential. However, the pathogenesis of DOR is still unclear and its treatment options are limited. This study aimed to explore DOR’s molecular mechanisms. Methods We used R software to analyze the mRNA microarray dataset E-MTAB-391 downloaded from ArrayExpress, screen for differentially expressed genes (DEGs), and perform functional enrichment analyses. We also constructed the protein-protein interaction (PPI) and miRNA-mRNA networks. Ovarian granulosa cells (GCs) from women with DOR and the control group were collected to perform untargeted metabolomics analyses. Additionally, small molecule drugs were identified using the Connectivity Map database. Results We ultimately identified 138 DEGs. Our gene ontology (GO) analysis indicated that DEGs were mainly enriched in cytokine and steroid biosynthetic processes. According to the Kyoto Encyclopedia of Genes and Genomes (KEGG), the DEGs were mainly enriched in the AGE (advanced glycation end-product)-RAGE (receptor for AGE) signaling pathway in diabetic complications and steroid biosynthesis. In the PPI network, we determined that JUN, EGR1, HMGCR, ATF3, and SQLE were hub genes that may be involved in steroid biosynthesis and inflammation. miRNAs also played a role in DOR development by regulating target genes. We validated the differences in steroid metabolism across GCs using liquid chromatography-tandem mass spectrometry (LC-MS/MS). We selected 31 small molecules with potentially positive or negative influences on DOR development. Conclusion We found that steroidogenesis and inflammation played critical roles in DOR development, and our results provide promising insights for predicting and treating DOR.