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- Title
ESTIMATION OF LIPOPROTEIN LIPASE ENZYME, APOLIPOPROTEIN E, APOLIPOPROTEIN C2 IN SMOKERS AND NONSMOKERS MALES.
- Authors
Hassan, Muthunna F.; Smaism, Maha F.; Alsalihi, Oday J.
- Abstract
Tobacco use is the most common cause of preventable cardiovascular mortality worldwide. Heavy smokers are variably defined by some studies suggest the exposure to two or more packets (e" 30 cigarettes) a day for 10 years or more. Lipoprotein lipase (LPL) is a hydrolysis enzyme that has a central role in plasma lipid metabolism, which hydrolysis the lipoproteins rich triglyceride, the aims of the study are investigation the causes of increasing LDL- cholesterol in heavy smokers males by measuring lipid cycle: Triglyceride (TG), very low density lipoprotein (VLDL), low density lipoprotein (LDL), Lipoprotein lipase (LPL) and its receptor, apo lipoprotein C2 (apo C2) and its receptor, apolipoprotein E (apoE) and its receptor, This study was included (87) males, their ages between (40-50 years) and body mass index is normal subjects (29 smokers without hypertension group A, 29 smoker with hypertension group B, 29 as a control group). The result showed a significantly increase in apo E, apoC2, apo C2 receptor, LPL receptor and lipid parameters (TG, VLDL-C, LDL-C) in both smokers groups (smokers, smoker with hypertension) when compared with control group, while significantly decreasedofLPL enzyme in smokers groups (A,B) when compared to control. In addition, the result observed there was no significant differences between study groups (control, group A and group B) according to apo E receptor. The results showed significant negative correlation between LPL concentration and (apo C2, TG, VLDL-C) in smokers groups (A, B) but the enzyme has a significant positive correlation with apo C2 in control group. In addition, there were a significant positive correlation between apo E and (TG, LDL-C) in smokers groups (A, B) but there were a significant negative correlation between apo E and (TG, LDL) in control group. In addition, there were a significant positive correlation between apo C2 and TG in smokers groups (A, B) but in control, the apo C2 has negative correlation with TG. Smoking is associated with increasing apo E that may altered VLDL size and my inhibit transferring of cholesterol to HDL resulting in increased LDL in smokers. The result showed a decrease LPL concentration that may be theprimary cause of hyperlipidemia, increase level of apo C2 may be caused as a response to decreasing LPL that trend to increase TG in smokers, increase LPL receptor may associating with hyperlipidemia by hampering the interaction between LPL and lipoprotein particles.
- Publication
Biochemical & Cellular Archives, 2018, Vol 18, Issue 1, p299
- ISSN
0972-5075
- Publication type
Academic Journal