<p>Full data.</p>

Associations between the investigated polymorphisms and T2DM were analyzed under codominant, dominant, recessive, and log-additive models, with adjustment for body mass index (BMI), waist-to-hip ratio (WHR), and family history of diabetes.</p> <p>Results</p><p>Both polymorphisms satisfied the Hardy-Weinberg equilibrium in the control group. For <i>IL16</i> rs11556218, significant differences in allele and genotype frequencies were observed between patients and controls, and the G allele showed a nominal association with lower odds of T2DM.

After adjustment for BMI, WHR, and family history of diabetes, the TG genotype showed a nominal association with lower odds of T2DM in the codominant model (adjusted OR = 0.56, 95% CI: 0.32–0.98; nominal P = 0.026). Nominal associations were also observed in the dominant model (adjusted OR = 0.52, 95% CI: 0.30–0.89; nominal P = 0.016) and the log-additive model (adjusted OR = 0.52, 95% CI: 0.32–0.85; nominal P = 0.0081).

For <i>IL1B</i> rs16944, genotype distribution likewise differed between the two groups. Under the recessive model, the CC genotype showed a nominal association with higher odds of T2DM after adjustment (adjusted OR = 2.13, 95% CI: 1.20–3.79; nominal P = 0.0089). None of these associations met the Bonferroni-corrected significance threshold of P < 0.00625.

Compared with controls, participants with T2DM had higher BMI and WHR, higher triglyceride levels, lower HDL cholesterol, higher fasting plasma glucose and blood pressure, and more commonly reported a family history of diabetes.</p> <p>Conclusions</p><p><i>IL16</i> rs11556218 and <i>IL1B</i> rs16944 showed nominal associations with T2DM in this sample of Kinh Vietnamese adults, although none remained statistically significant after Bonferroni correction.

These exploratory findings require confirmation in larger independent studies before any firm conclusions regarding their biological or clinical relevance can be drawn.</p></div>