Omer Atis1, Semsettin Sahin2, Koksal Ceyhan3, Huseyin Ozyurt2, Ali Akbas2, Ismail Benli2. 1. Department of Medical Biology, Atatürk University School of Medicine, Erzurum, Turkey. 2. Department of Biochemistry, Gaziosmanpaşa University School of Medicine, Tokat, Turkey. 3. Department of Cardiology, Gaziosmanpaşa University School of Medicine, Tokat, Turkey.
Abstract
OBJECTIVE: Coronary artery disease (CAD) is a multifactorial disease that is caused by various genetics and environmental factors. Genetically, predisposition is an important component for CAD. The candidate apolipoprotein E (apoE) gene is the most studied one. ApoE is composed of e2, e3, e4 alleles and E2/2, E2/3, E2/4, E3/3, E3/4, E4/4 genotypes. In this study, the relationship between CAD and apoE polymorphism and apoE level has been studied in Tokat region. MATERIALS AND METHODS: The study population is composed of 100 CAD patients diagnosed by coronary angiography and 100 control patients of whom fifty have normal coronary angiography and fifty did not have any CAD symptoms. The serum lipid and apoE levels and apoE genotypes of all participants have been measured, and the relationship between these parameters has been evaluated. RESULTS: Apolipoprotein E, total cholesterol, HDL cholesterol and LDL cholesterol levels were statistically low at CAD patients than control patients (p=0.0004, p=0.0005, p=0.0107, p=0.0052 respectively). There was not any significant difference between triglyceride levels (p=0.0848). Waist circumferences were significantly high at CAD patients (p=0.0012). Allele frequencies were as e2 (7.25%), e3 (83.5%), e4 (9.25%) and genotype distributions were as E2/2 (0.5%), E2/3 (13%), E2/4 (0.5%), E3/3 (68.5%), E3/4 (16.5%), E4/4 (1%). The distribution of alleles and genotypes were not significantly different (p>0.05). ApoE levels were higher at e2 allele carriers than e3 and e4 allele carriers (p<0.05). However, there was no significant difference between e3 and e4 allele carriers. CONCLUSION: In conclusion, the distribution of apoE genotype and allele at our region is similar to the general of Turkey. The low apoE levels in CAD patients may show the influence of apoE on CAD by local and systemic mechanisms.
OBJECTIVE:Coronary artery disease (CAD) is a multifactorial disease that is caused by various genetics and environmental factors. Genetically, predisposition is an important component for CAD. The candidate apolipoprotein E (apoE) gene is the most studied one. ApoE is composed of e2, e3, e4 alleles and E2/2, E2/3, E2/4, E3/3, E3/4, E4/4 genotypes. In this study, the relationship between CAD and apoE polymorphism and apoE level has been studied in Tokat region. MATERIALS AND METHODS: The study population is composed of 100 CAD patients diagnosed by coronary angiography and 100 control patients of whom fifty have normal coronary angiography and fifty did not have any CAD symptoms. The serum lipid and apoE levels and apoE genotypes of all participants have been measured, and the relationship between these parameters has been evaluated. RESULTS:Apolipoprotein E, total cholesterol, HDL cholesterol and LDL cholesterol levels were statistically low at CAD patients than control patients (p=0.0004, p=0.0005, p=0.0107, p=0.0052 respectively). There was not any significant difference between triglyceride levels (p=0.0848). Waist circumferences were significantly high at CAD patients (p=0.0012). Allele frequencies were as e2 (7.25%), e3 (83.5%), e4 (9.25%) and genotype distributions were as E2/2 (0.5%), E2/3 (13%), E2/4 (0.5%), E3/3 (68.5%), E3/4 (16.5%), E4/4 (1%). The distribution of alleles and genotypes were not significantly different (p>0.05). ApoE levels were higher at e2 allele carriers than e3 and e4 allele carriers (p<0.05). However, there was no significant difference between e3 and e4 allele carriers. CONCLUSION: In conclusion, the distribution of apoE genotype and allele at our region is similar to the general of Turkey. The low apoE levels in CAD patients may show the influence of apoE on CAD by local and systemic mechanisms.
Authors: June E Eichner; S Terence Dunn; Ghazala Perveen; David M Thompson; Kenneth E Stewart; Berrit C Stroehla Journal: Am J Epidemiol Date: 2002-03-15 Impact factor: 4.897
Authors: J A Kuivenhoven; J W Jukema; A H Zwinderman; P de Knijff; R McPherson; A V Bruschke; K I Lie; J J Kastelein Journal: N Engl J Med Date: 1998-01-08 Impact factor: 91.245
Authors: R W Mahley; K E Palaoğlu; Z Atak; J Dawson-Pepin; A M Langlois; V Cheung; H Onat; P Fulks; L L Mahley; F Vakar Journal: J Lipid Res Date: 1995-04 Impact factor: 5.922
Authors: J E Eichner; L H Kuller; T J Orchard; G A Grandits; L M McCallum; R E Ferrell; J D Neaton Journal: Am J Cardiol Date: 1993-01-15 Impact factor: 2.778
Authors: Alexander M Kulminski; Konstantin G Arbeev; Irina Culminskaya; Liubov Arbeeva; Svetlana V Ukraintseva; Eric Stallard; Kaare Christensen; Nicole Schupf; Michael A Province; Anatoli I Yashin Journal: PLoS Genet Date: 2014-01-30 Impact factor: 5.917
Authors: Yanal A Shafagoj; Randa G Naffa; Mohammed S El-Khateeb; Yazeed L Abdulla; Aseem A Al-Qaddoumi; Faisal A Khatib; Yousef F Al-Motassem; Eman M Al-Khateeb Journal: Neurosciences (Riyadh) Date: 2018-01 Impact factor: 0.906