Monocyte chemoattractant protein-1 (MCP-1) participates in the initiation and progression of atherosclerosis. In vitro studies have reported that the MCP-1 rs1024611 polymorphism is associated with increased MCP-1 concentrations. The study aimed to define whether MCP-1 concentrations are associated with premature coronary artery disease (pCAD) and to establish whether variations in the rs1024611 polymorphism increase MCP-1 concentrations. MCP-1 rs1024611 polymorphism was determined in 972 pCAD patients and 1070 control individuals by real-time PCR. MCP-1 concentrations were determined by the Bio-Plex system. In the total population, men had higher MCP-1 concentrations when compared to women (p < 0.001). When stratified by rs1024611 genotypes, higher MCP-1 concentrations were observed in AA individuals compared to GG subjects (p = 0.023). When performing the analysis considering sex, the differences remained significant in women (AA vs. GG, p = 0.028 and GA vs. GG, p = 0.008). MCP-1 concentrations were similar in pCAD patients and controls (p = 0.782). However, the independent analysis of the studied groups showed that in patients with the AA genotype, MCP-1 concentrations were significantly higher when compared to patients with the GG genotype (p = 0.009). Considering that the AA genotype increases MCP-1 concentration, we evaluated whether, in AA genotype carriers, MCP-1 concentrations were associated with pCAD. The results showed that for every ten pg/mL increase in MCP-1 concentration, the risk of presenting pCAD increases by 2.7% in AA genotype individuals. Individuals with the MCP-1 rs1024611 AA genotype present an increase in MCP-1 concentration. In those individuals, increased MCP-1 concentrations increase the risk of presented pCAD.

Interleukin 6 (IL-6) is a cytokine implicated in the development of atherosclerosis. This study aimed to determine the association of three IL-6 gene polymorphisms with increased carotid intima-media thickness (CIMT) and cardiometabolic risk factors. Three IL-6 polymorphisms (rs1800795, rs2069827, and rs1800796) were analyzed in 178 individuals with increased CIMT (CIMT ≥ 75th percentile) and 906 individuals without increased CIMT (CIMT < 75th percentile). Logistic regression, adjusted for confounding variables, was employed to assess the associations. The rs1800796 polymorphism was significantly associated with an elevated risk of increased CIMT (OR = 1.354, Padditive = 0.016; OR = 1.803, Precessive = 0.014; OR = 1.989, Pcodominant2 = 0.008). One haplotype (GCG) correlated with a higher risk of increased CIMT (OR = 1.288; P = 0.008), while another (GGG) demonstrated a reduced risk (OR = 0.773; P = 0.006). In individuals without increased CIMT, the rs2069827 polymorphism was associated with low risks of central obesity, hypoalphalipoproteinemia, and a low risk of presenting with high levels of total cholesterol (TC), non-high-density lipoprotein cholesterol (non-HDL-C), low-density lipoprotein cholesterol (LDL-C) /HDL-C index, apolipoprotein B, and gamma-glutamyl transpeptidase. The rs1800796 polymorphism was associated with a low risk of adipose tissue insulin resistance, and the rs1800795 was associated with a minimal risk of central obesity and hypoalphalipoproteinemia. Among those with increased CIMT, the rs2069827 was associated with low risks of central obesity, hypertriglyceridemia, metabolic syndrome, and a high triglyceride (TG)/HDL-C index, while rs1800796 was associated with a low risk of fatty liver. Similar IL-6 concentrations were observed in both individuals with and without increased CIMT. In conclusion, the rs1800796 polymorphism is associated with increased CIMT, while the rs2069827 and rs1800795 are linked to cardiovascular risk factors.

Dipeptidyl peptidase-4 (DPP4) concentrations are known to correlate with nonalcoholic fatty liver (FL), which is also associated with subclinical atherosclerosis (SA). This study aimed to determine whether DPP4 concentrations and the DPP4 rs17574 polymorphism are associated with FL in individuals with SA. The study included 378 participants with SA, of whom 143 had FL and 235 did not. DPP4 serum concentrations were measured using a Bioplex system, and DPP4 rs17574 genotypes were determined using TaqMan assays. Logistic regression was used to assess the relationships between FL, DPP4 concentrations, and rs17574 genotypes. Overall, DPP4 concentrations did not differ significantly between individuals with and without FL. No significant differences in DPP4 levels were observed among DPP4 genotypes in the total sample. However, within the FL group, significant differences in DPP4 concentration were observed across genotypes: AA genotype (134 [106–175] ng/mL), AG genotype (128 [114–149] ng/mL), and GG genotype (80 [71–117] ng/mL); P = 0.019. The DPP4 rs17574 polymorphism was associated with FL under a recessive model (P = 0.037). DPP4 concentration was also significantly associated with FL: the likelihood of presenting with FL increased by 6.2% for every 10 ng/mL increase in DPP4 levels (P = 0.009). These findings suggest that DPP4 concentration may serve as a biochemical risk marker for FL in individuals with SA. Moreover, the rs17574 polymorphism may influence DPP4 protein levels, particularly in those with FL. To our knowledge, this is the first study to describe an association between DPP4 concentration, the rs17574 polymorphism, and FL. Assessing DPP4 levels may offer a novel and effective strategy for risk stratification of FL in SA populations.