Association of ABO Gene rs2073823 Polymorphism with Microvascular Complications, sP-Selectin Levels and Lipid Profile in Type 2 Diabetes.

Introduction: Type 2 diabetes (T2D) is a prevalent metabolic disorder linked to chronic inflammation and endothelial dysfunction, which contributes to the development of microvascular complications (MVCs) such as diabetic retinopathy (DR) and diabetic neuropathy (DN). Genetic factors, including variations in the ABO gene, may influence these complications. This study aimed to investigate the association between the ABO rs2073823 polymorphism and the risk of MVCs in patients with T2D, as well as its impact on inflammatory biomarkers, endothelial markers, and lipid profiles.

Materials and methods: We conducted an exploratory study involving 96 T2D Iraqi patients (Asian Arabic), examining the distribution of the ABO rs2073823 polymorphism and its correlation with MVCs. We assessed levels of inflammatory markers (TNF-α, IL-6, sE-selectin, sP-selectin), glycemic markers, renal function biomarkers, and lipid profiles. Adjustment was made for confounding factors including age, gender, body mass index, duration of diabetes, and hypertension.

Results: Among the participants, 75% had MVCs, including DR (42%) and DN (65%). The ABO rs2073823 "A/A" genotype was associated with a reduced risk of MVCs under co-dominant (OR=0.16, p=0.045) and recessive models (OR=0.14, p=0.031). This protective effect remained significant after adjusting for confounding factors (OR=0.11, p=0.022). The "A/A" genotype was also linked to lower levels of total cholesterol, LDL-cholesterol, triglycerides, and sP-selectin. Patients with MVCs exhibited significantly higher levels of TNF-α, IL-6, and sP-selectin.

Conclusion: The ABO rs2073823 polymorphism, particularly the "A/A" genotype, is associated with a decreased risk of MVCs in T2D patients and influences lipid metabolism and inflammatory markers. These findings suggest a genetic basis for the susceptibility to MVCs and highlight the role of the ABO gene in modulating inflammation and endothelial function in T2D. Further research is needed to validate these associations and explore potential therapeutic implications.