Impact of Promotor region Cdx2 (A/G) Variant of Vitamin-D Receptor Gene on Omentin-1, Leptin levels and Coronary Artery Risk in Pakistani Cohorts

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Objectives: Coronary artery disease remains a major contributor to global morbidity and mortality, primarily driven by atherosclerosis. Genetic variations and adipocytokines like omentin-1 and leptin play critical roles in inflammatory pathways and atherosclerotic processes. This study aims to evaluate the association of Cdx2 (A>G) variant, omentin-1 and leptin with CAD risk in a Pakistani population. Methods: This case-control study comprised 500 angiographically confirmed CAD patients and 500 age- and gender-matched healthy controls. Detailed anthropometric measurements, blood pressure and fasting blood samples were obtained from all contributors. Genotyping of the Cdx2 (A>G) variant was conducted using tetra-primer amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). Serum levels of omentin-1, leptin and vitamin-D were evaluated by using enzyme-linked immunosorbent assay (ELISA) kits. Statistical analyses was done by SPSS version 23. Results: The frequency of the AA genotype in the control group (49.2%) was significantly higher than in CAD patients (32.4%), indicating a protective effect (p<0.001). The AG genotype was associated with a 58% increased risk of CAD (OR = 1.58, 95% CI: 1.24-2.02). Serum omentin-1 levels were significantly lower in CAD patients (368±3.7 ng/mL vs. 615±6.5 ng/mL, p<0.001) compared to controls, whereas, leptin levels were significantly elevated in CAD patients (8.62±0.7 ng/mL vs. 4.02±0.5 ng/mL, p<0.001). Both omentin-1 and leptin levels were significantly associated with the AG and GG genotypes, suggesting a genetic influence on these adipocytokine. Conclusion: In conclusion Cdx2 (A>G) variant of promotor region of VDRG was found to be associated with greater risk of CAD and also influence on adipokines levels, particularly omentin-1 and leptin, may play a crucial role in CAD pathogenesis. These findings offer insights into the molecular mechanisms of CAD.

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