Association of Apelin gene rs3115757 variation and expression with metabolic syndrome among female students in King Abdulaziz University
Gene Reports, ISSN: 2452-0144, Vol: 24, Page: 101305
2021
- 12Captures
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Metrics Details
- Captures12
- Readers12
- 12
Article Description
Metabolic syndrome (MetS) is a cluster of medical components that, when occurring together, increase the risk of heart disease, stroke, and type 2 diabetes. This syndrome is widespread around the world, affecting over one billion individuals according to recent reports. Abdominal obesity is a cornerstone of MetS. Apelin is an endogenous peptide and a member of the adipokine family that exhibits a positive correlation with obesity. In this study, we analyzed data on a total of 160 healthy female students aged 18–25 years to estimate the contributions of the apelin gene variant to MetS components in female students at King Abdulaziz University. APLN gene rs3115757 (C < G) was genotyped using TaqMan SNP genotyping assay. ELISA technique was performed on serum to detect; apelin, Insulin Resistance (HOMA-IR), fasting blood glucose (FG), triglycerides (TG) and high-density lipoprotein (HDL), serum triglycerides and glucose concentrations were colorimetric determined. Body mass index (BMI), waist circumference (WC), systolic and diastolic blood pressures (SBP/DBP) were also measured and compared among subjects. The association between the genotype distribution and MetS risk was evaluated using Chi-square test of independence. No significant difference was recorded in apelin levels between MetS and control groups, however, significant differences were recorded in TG, FG, HOMA-IR, WC, and BMI ( p < 0.005) between the control and MetS subjects. We also recorded an increase in the frequency of APLN gene rs3115757 variant, however it wasn't significantly associated with an increased risk of MetS. Further investigation on the apelin rs3115757 polymorphism is needed to draw a firm conclusion about its association with the risk of MetS in different ethnicities.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2452014421002909; http://dx.doi.org/10.1016/j.genrep.2021.101305; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85111955974&origin=inward; https://linkinghub.elsevier.com/retrieve/pii/S2452014421002909; https://dx.doi.org/10.1016/j.genrep.2021.101305
Elsevier BV
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