ABSTRACT
BACKGROUND: The association between Apolipoprotein A5 (APOA5) genetic polymorphisms and susceptibility to metabolic syndrome (MetS) has been established by many studies, but there have been conflicting results from the literature. We performed a meta-analysis of observational studies to evaluate the association between APOA5 gene polymorphisms and the prevalence of MetS. METHODS: PubMed, Web of Science, Embase, and Scopus were searched up to April 2024. The random effects model was used to estimate the odds ratios (ORs) and 95% confidence intervals (CI) of the association between APOA5 gene polymorphisms and the prevalence of MetS development. The potential sources of heterogeneity were evaluated by subgroup analyses and sensitivity analyses. RESULTS: A total of 30 studies with 54,986 subjects (25,341 MetS cases and 29,645 healthy controls) were included. The presence of rs662799 and rs651821 polymorphisms is associated with an approximately 1.5-fold higher likelihood of MetS prevalence (OR = 1.42, 95% CI: 1.32, 1.53, p < 0.001; I2 = 67.1%; P-heterogeneity < 0.001; and OR = 1.50, 95% CI: 1.36-1.65, p < 0.001), respectively. MetS is also more prevalent in individuals with the genetic variants rs3135506 and rs2075291. There was no evidence of a connection with rs126317. CONCLUSION: The present findings suggest that polymorphisms located in the promoter and coding regions of the APOA5 gene are associated with an increased prevalence of MetS in the adult population. Identifying individuals with these genetic variations could lead to early disease detection and the implementation of preventive strategies to reduce the risk of MetS and its related health issues. However, because the sample size was small and there was evidence of significant heterogeneity for some APOA5 gene polymorphisms, these results need to be confirmed by more large-scale and well-designed studies.
Subject(s)
Apolipoprotein A-V , Genetic Predisposition to Disease , Metabolic Syndrome , Polymorphism, Single Nucleotide , Metabolic Syndrome/genetics , Metabolic Syndrome/epidemiology , Apolipoprotein A-V/genetics , Humans , Odds RatioABSTRACT
Curcumin-containing soy protein nanoparticles (curcumin-SPNs) were synthesized by desolvation (coacervation) method and characterized by SEM, DLS, FTIR, and XRD. For anticancer evaluation, osteogenic sarcoma (SAOS2) cell lines were incubated with different concentrations of nanostructures. The dialysis method was used for assessment of drug release. Intracellular reactive oxygen species (ROS) were evaluated in IC50 dose after 24 h of exposure to free curcumin and curcumin-SPNs. Characterization data showed that the size of drug-free SPNs and curcumin-SPNs were 278.2 and 294.7 nm, respectively. The zeta potential of drug-free SPNs and curcumin-SPNs were - 37.1 and - 36.51 mv, respectively. There was no significant difference between the control and drug-free SPNs groups in terms of cell viability (p > 0.05). The viability of cells in different concentrations of the designed curcumin-SPNs in Saos2 cell line was significantly higher than free drug (p < 0.05). The release of curcumin showed that more than 50% of the drug was released in the first 2 h of incubation. After this time, the slow release of drug was continued to 62-83% of drug. IC50 values of free curcumin and curcumin-SPNs (1/10) were 156.8 and 65.9 µg/mL, respectively (a free curcumin IC50 was 2.4 times more than curcumin-SPNs). Slow-release of the curcumin causes the cell to be exposed to the anticancer drug for a longer period of time. The intracellular ROS levels significantly increased in an IC50 dose after 24 h of exposure to both free curcumin and curcumin-SPNs compared with controls (p < 0.05).
