تقدير انزيم اللايييز الدهني، اييولييويروتين E واييولييويروتين C2 في الذكور المدخنين وغيرفي الذكور المدخنين وغير == Estimation of Lipoprotein Lipase Enzyme, Apolipoprotein E and Apolipoprotein C2 in Smokers and Nonsmokers Males in Hilla city
Author name:
مثنى فليح حسن جلوب
Supervisor name:
مها فاضل سميسم | عدي جاسم الصالحي
General topic:
Medicine
Specific topic:
Clinical Biochemistry
Degree:
Master
University:
University of Babylon - Faculty Of Medicine
Language:
English
University location:
Babylon
First pages:
19T1716 - p.pdf
Abstract:
moking is associated with an increase circulating low - density lipoprotein cholesterol (LDL - C), plasma triglycerides (TGs) and very lowdensity lipoprotein (VLDL) levels.The aim of this study is to investigate the cause of increasing (LDL) level in smoking men by measuring lipoprotein lipase (LPL), lipoprotein lipase receptor, apolipoprotein C2 (apoC2), apolipoprotein C2 receptor, apolipoprotein E (apo E), apo E receptor, (TG), (VLDL) and (LDL). To achieve this aim (87) men were included in this study, their ages between (40 - 50) years with normal body mass index. (58) of them were heavy smokers who smoked one to two packets (≥ 30 cigarettes per day for 10 years), (29) smokers (group A) without hypertension were included. The other (29) men were smokers with hypertension (group B), while the other (29) men were the control group. The sera sample of all groups were used to measure the concentration of lipid parameters TG, VLDL and LDL byusing colorimetric methods, and ELISA method for determination of LPL, LPL receptor, apo C2, apo C2 receptor, apo E and, apo E receptor. The results of the present study show : There is a significant increase (P <0.001) in mean of TG, VLDL and LDL - C in group (A) and (B) when compared to the control group, in addition, there is a significant increase in the mean of TG, LDL (p=0.05, P=0.015) respectively in the smoking group (B) when compared to group (A). The result showed there were no significant differences in mean of VLDL - C between group (A) and (B) (P=0.26). There is a significant decrease in the mean of LPL in groups (A, B) (p <0.001, P=0.011) respectively when compared to the control group. In addition, there is a significant increase in the mean of LPL in group (B) when compared to group (A) (P =0.02).There is a significant increase in the mean of lipoprotein lipase receptor in groups (A, B) (p=0.005, P=0.012) respectively when compared to the control group, and there are no significant differences in LPL receptor between group (A) and group (B) (P=0.66).There is a significant increase in the mean of apo C2 in group (A) and (B) (p<0.001, P=0.028) respectively, when compared to the control group, and there are no significant differences in the mean of apo C2 between groups (A) and (B) (P=0.85).There is a significant increase in the mean of apo C2 receptor in groups (A, B) (p=0.004, P=0.017) respectively, when compared to the control group, and there are no significant differences in the mean of apo C2 receptor between groups (A) and (B) (P=0.62).There is a significant increase in the mean of apo E in groups (A, B) (p=0.002, P<0.001) respectively, when compared to the control group. In addition, there are no significant differences in the mean of apo E between groups (A) and (B) (P=0.94).There is no significant differences in the mean of apo E receptor in study groups (A), (B) and control There is a significant negative correlation between LPL and TG in the control group (P<0.001, r = - 0.635) and in group (A) (P=0.001, r= - 0.498), but there is no significant correlation between LPL and TG level in group (B) (P=0.076, r = - 0.329).A significant negative correlation is found between LPL and VLDL control group (P<0.001, r= - 0.611), group A (P=0.002, r = - 0.546) and group B (P=0.004, r = - 0.513).There is a significant positive correlation between LPL and apo C2 in control group (P=0.022, r= 0.469). In addition, there is a significant negative correlation between LPL and apo C2 in group A (P=0.038, r = - 0.388) and there is no significant correlation in group (B) (P=0.070, r = - 0.341). There is a significant negative correlation of apo C2 with TG in control group (P=0.003, r = - 0.529). In addition, there is a significant positive correlation between apo C2 and TG in group A (P=0.011, r=0.464), and group B (P=0.004, r=0.508).There is a significant negative correlation of apo E with LDL in the control group (P=0.008, r = - 0.474). In addition, there is a significant positive correlation between apo E and LDL in group A (P=0.041, r =0.399) and group B (P<0.001, r =0.660).There is a significant negative correlation between apo E and TG in the control group (P=0.012, r = - 0.461). In addition, there is a significant positive correlation between apo E and TG in group A (P=0.034, r =0.395), and there is no significant correlation between apo E and TG in group (B) (P=0.079, r =0.325).The study concludes that smoking is as sociated with increase Apo E level that may alter VLDL resulting to increase LDL, also shows that the decreased level of LPL is related to smoking that causes hypertriglyceridemia and increasing Apo C2 as a response to enzyme deficiency. LPL receptor increased in smoking leading to decrease bindingof LPL to its legend lipoprotein.
