Effect of Plasminogen Activator Inhibitor-1 and Tissue Plasminogen Activator Polymorphisms on Susceptibility to Type 2 Diabetes in Malaysian Subjects

Table 2

Association of PAI-1 4G/5G polymorphisms with type 2 diabetes mellitus in Malaysian subjects.

PAI-1 4G/5G polymorphism	Control (𝑛=131)	Type 2 diabetes mellitus		Total type 2 diabetes mellitus (𝑛=303)
		Without MetS; (𝑛=76)	With MetS; (𝑛=227)
Risk allele frequency (4G)	0.47	0.48	0.49	0.50
(4G/4G)/(4G/5G)/(5G/5G) (frequency)	0.23/0.485/0.29	0.25/0.54/0.21	0.25/0.48/0.27	0.25/0.50/0.25
Recessive model	Odds ratio	1.8	0.66	0.78
	95% CI	(0.77–4.2)	(0.31–1.4)	0.37–1.66
	𝑃 value	0.17	0.29	0.52
Dominant model	Odds ratio	2.35	1.61	1.5
	95% CI	1.0–5.43	(0.9–2.91)	0.72–1.7
	𝑃 value	0.045	0.11	0.28
Additive model	Odds ratio	1.67	1.1	1.1
	95% CI	0.98–2.84	0.75–1.6	0.69–1.74
	𝑃 value	0.058	0.63	0.69

In the additive model, genotype of homozygote for the nonrisk allele 5G/5G (0/0), heterozygote 4G/5G (1/0), and homozygote for the risk allele 4G/4G (1/1) were coded as 0, 1, and 2, respectively. The recessive model was defined as 4G/4G versus (4G/5G + 5G/5G), dominant model as (4G/4G + 4G/5G) versus 5G/5G, and additive model as 4G/4G versus 4G/5G versus 5G/5G. The results presented odds ratio, 95% CI, and 𝑃 value adjusted for age, gender, race, family history of diabetes, and BMI as covariates which evaluated by hierarchical logistic regression. MetS: metabolic syndrome.