Abstract

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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.