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Variants of the interleukin-1β (IL-1β) gene have been associated with type 2 diabetes (T2D) and coronary artery diseases (CAD). However, association of IL-1β polymorphisms with diabetic patients having CAD clinical manifestation has not been studied yet. In this study, we aim to decipher the role of IL-1β common promoter variants with susceptibility/resistance to development of CAD in T2D patients. T2D patients with (n = 134) or without CAD (n = 533) were enrolled. A total of 513 essentially healthy individuals from the same population were included in this study as control. Plasma levels of IL-1β were quantified by enzyme-linked immunosorbent assay (ELISA) kit as per instructions from the manufacturer. IL-1β promoter variants (T-31C and C-511T) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). T2D patients displayed higher level of plasma IL-1β in comparison to healthy controls. Prevalence of variants for IL-1β (C-511T) polymorphism was higher in diabetic patients compared to controls (CT: P < 0.0001, OR = 3.01; TT: P < 0.0001, OR = 2.45). IL-1β (C-511T) polymorphism was linked with plasma IL-1β levels. Interestingly, heterozygous mutants (CT) were most prevalent in T2D individuals with CAD compared to those without CAD (P = 0.03, OR = 1.82). Furthermore, low-density lipoprotein (LDL) and triglycerides were elevated in T2D patients with CAD than in patients without heart-related disorder. No significant association of other polymorphism (T-31C) was noticed with susceptibility to T2D or diabetic patients with heart disorders. IL-1β (C-511T) variants are associated with elevated plasma IL-1β levels. Mutation at the IL-1β promoter region (C-511T) predisposed subjects to the development of T2D and CAD manifestation in diabetic patients. [ABSTRACT FROM AUTHOR]

Variants of the interleukin-1β (IL-1β) gene have been associated with type 2 diabetes (T2D) and coronary artery diseases (CAD). However, association of IL-1β polymorphisms with diabetic patients having CAD clinical manifestation has not been studied yet. In this study, we aim to decipher the role of IL-1β common promoter variants with susceptibility/resistance to development of CAD in T2D patients. T2D patients with (n = 134) or without CAD (n = 533) were enrolled. A total of 513 essentially healthy individuals from the same population were included in this study as control. Plasma levels of IL-1β were quantified by enzyme-linked immunosorbent assay (ELISA) kit as per instructions from the manufacturer. IL-1β promoter variants (T-31C and C-511T) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). T2D patients displayed higher level of plasma IL-1β in comparison to healthy controls. Prevalence of variants for IL-1β (C-511T) polymorphism was higher in diabetic patients compared to controls (CT: P < 0.0001, OR = 3.01; TT: P < 0.0001, OR = 2.45). IL-1β (C-511T) polymorphism was linked with plasma IL-1β levels. Interestingly, heterozygous mutants (CT) were most prevalent in T2D individuals with CAD compared to those without CAD (P = 0.03, OR = 1.82). Furthermore, low-density lipoprotein (LDL) and triglycerides were elevated in T2D patients with CAD than in patients without heart-related disorder. No significant association of other polymorphism (T-31C) was noticed with susceptibility to T2D or diabetic patients with heart disorders. IL-1β (C-511T) variants are associated with elevated plasma IL-1β levels. Mutation at the IL-1β promoter region (C-511T) predisposed subjects to the development of T2D and CAD manifestation in diabetic patients. [ABSTRACT FROM AUTHOR]