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Association between HindIII (rs320) variant in the lipoprotein lipase gene and the presence of coronary artery disease and stroke among the Saudi population
Institution:1. Department of Medical Genetics, Faculty of Medicine, Umm Al-Qura University (UQU), Saudi Arabia;2. Department of Cardiology, King Abdulla Medical city, Makkah, Saudi Arabia;3. Department of Cardiology, Dalhousie University Halifax, Nova Scotia, Canada;4. Department of Cardiac Surgery, King Fahd Armed Medical Forces Hospitals, Jeddah, KSA, Saudi Arabia;5. Department of Cardiac Surgery, Monzino Heart Center, University of Milan, Milan, Italy;6. Biochemistry Department, Faculty of medicine, UQU, Saudi Arabia;7. Faculty of Medicine, Ain-Shams University, Egypt;8. Biomedical Sciences, University of Brighton, England, UK;9. Science and technology Unit, UQU, Saudi Arabia;10. Department of Internal Medicine, College of Medical Sciences, University of Maiduguri, Nigeria;11. Clinical Pathology Department, Faculty of Medicine, Zagazig University, Egypt;12. School of Pharmacy, University of Brighton, England, UK
Abstract:Lipoprotein Lipase (LPL) is known to be a key enzyme for lipid metabolism specifically in an enzymatic glycoprotein which provide tissues without fatty-acids and eliminates triglycerides (TG) by the circulation. Mutations in LPL were proven to cause alteration in fractions within lipoprotein, causing the development of atherosclerosis which predispose to weakening coronary artery disease (CAD) and stroke. We examined the linkage between genetic variant HindIII in LPL on lipoprotein fractions, stroke occurrences and CAD. In this case-control study, we have recruited 315 CAD cases and 205 age-matched controls. A total of 520 genomic DNA was digested with the purified PCR products for restriction fragment length polymorphism with HindIII restriction enzyme. The distribution of genotypes in a decreasing order were TT, 148 (47%), GT 135 (42.9%) and GG 32 (10.2%) in CAD groups of the study while the pattern in controls were GT 91 (44.4%), TT 86 (42%) and GG 28 (13.7%). None of all the allele or genotype frequencies were found to be significant in our study (p greater than 0.05), while the biochemical levels for both TG and LDL-c were shown to be prone in CAD patients when compare with the controls. Furthermore, the occurence of strokes were more in CAD groups vs. controls: 72 (22.9%) vs. 7 (3.4%) p 0.000]. This could indicate the influence of HindIII variant on plasma lipid levels, and the possibility of considering it a risk factor for atherosclerosis leading to CAD and stroke occurrence.
Keywords:Coronary artery disease  Stroke  Lipoprotein lipase
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