Association of the lipoprotein lipase and Apolipoprotein C-II gene polymorphisms with risk of dyslipidemia in smokers and non-smokers male

Objective: Dyslipidaemia is considered a metabolic abnormality andan important risk factor that leads to atherogenic cardiovascular diseases. Cigarette smoking is associated with dyslipidaemia. This study aimed to demonstrate whether lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) gene polymorphisms can be considered as independent genetic risk factors for dyslipidaemia among smokers with various smoking durations. Methods: A total of 185 males (90 smokers and 95 non-smokers)were included in this study, Lipid profiles were measured and DNA was isolated. The LPL-Hind III and APO CII-Ava II polymorphisms were determined using the polymerase reaction-restriction fragment length polymorphisms (RFLP) technique. Results: For the LPL-Hind IIIpolymorphism H+H+ genotype group, the triglycerides TG and very-low-density lipoprotein cholesterol VLDL-C concentrations were significantly higher and the high-density lipoprotein cholesterol HDL-C concentration was significantly lower than those of the H-H-genotype. ForAPO CII-Ava II polymorphisms, compared with those of the A2A2 genotype group, the total cholesterol TC, TG, low-density lipoprotein cholesterol LDL-C and VLDL-C concentrations were significantly increased in the A1A2 genotype group, while the HDL-C concentration was significantly decreased. Conclusions: The study revealed that the H+H+ or H +H-genotype of the LPL-Hind III polymorphism and the A1A1or A1A2 genotype of the APOCII-Ava II polymorphism were at higher risk of developing dysli-pidaemia compared to the H -H-genotype of the LPL-Hind III polymorphism and A2A2 genotype of the APOCII-Ava II polymorphism. (C) 2021 Cardiological Society of India. Published by Elsevier B.V. Objective: Dyslipidaemia is considered a metabolic abnormality andan important risk factor that leads to atherogenic cardiovascular diseases. Cigarette smoking is associated with dyslipidaemia. This study aimed to demonstrate whether lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) gene polymorphisms can be considered as independent genetic risk factors for dyslipidaemia among smokers with various smoking durations. Methods: A total of 185 males (90 smokers and 95 non-smokers)were included in this study, Lipid profiles were measured and DNA was isolated. The LPL-Hind III and APO CII-Ava II polymorphisms were determined using the polymerase reaction-restriction fragment length polymorphisms (RFLP) technique. Results: For the LPL-Hind IIIpolymorphism H+H+ genotype group, the triglycerides TG and very-low-density lipoprotein cholesterol VLDL-C concentrations were significantly higher and the high-density lipoprotein cholesterol HDL-C concentration was significantly lower than those of the H-H-genotype. ForAPO CII-Ava II polymorphisms, compared with those of the A2A2 genotype group, the total cholesterol TC, TG, low-density lipoprotein cholesterol LDL-C and VLDL-C concentrations were significantly increased in the A1A2 genotype group, while the HDL-C concentration was significantly decreased. Conclusions: The study revealed that the H+H+ or H +H-genotype of the LPL-Hind III polymorphism and the A1A1or A1A2 genotype of the APOCII-Ava II polymorphism were at higher risk of developing dysli-pidaemia compared to the H -H-genotype of the LPL-Hind III polymorphism and A2A2 genotype of the APOCII-Ava II polymorphism. (C) 2021 Cardiological Society of India. Published by Elsevier B.V. Objective: Dyslipidaemia is considered a metabolic abnormality andan important risk factor that leads to atherogenic cardiovascular diseases. Cigarette smoking is associated with dyslipidaemia. This study aimed to demonstrate whether lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) gene polymorphisms can be considered as independent genetic risk factors for dyslipidaemia among smokers with various smoking durations. Methods: A total of 185 males (90 smokers and 95 non-smokers)were included in this study, Lipid profiles were measured and DNA was isolated. The LPL-Hind III and APO CII-Ava II polymorphisms were determined using the polymerase reaction-restriction fragment length polymorphisms (RFLP) technique. Results: For the LPL-Hind IIIpolymorphism H+H+ genotype group, the triglycerides TG and very-low-density lipoprotein cholesterol VLDL-C concentrations were significantly higher and the high-density lipoprotein cholesterol HDL-C concentration was significantly lower than those of the H-H-genotype. ForAPO CII-Ava II polymorphisms, compared with those of the A2A2 genotype group, the total cholesterol TC, TG, low-density lipoprotein cholesterol LDL-C and VLDL-C concentrations were significantly increased in the A1A2 genotype group, while the HDL-C concentration was significantly decreased. Conclusions: The study revealed that the H+H+ or H +H-genotype of the LPL-Hind III polymorphism and the A1A1or A1A2 genotype of the APOCII-Ava II polymorphism were at higher risk of developing dysli-pidaemia compared to the H -H-genotype of the LPL-Hind III polymorphism and A2A2 genotype of the APOCII-Ava II polymorphism. (C) 2021 Cardiological Society of India. Published by Elsevier B.V. Objective: Dyslipidaemia is considered a metabolic abnormality andan important risk factor that leads to atherogenic cardiovascular diseases. Cigarette smoking is associated with dyslipidaemia. This study aimed to demonstrate whether lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) gene polymorphisms can be considered as independent genetic risk factors for dyslipidaemia among smokers with various smoking durations. Methods: A total of 185 males (90 smokers and 95 non-smokers)were included in this study, Lipid profiles were measured and DNA was isolated. The LPL-Hind III and APO CII-Ava II polymorphisms were determined using the polymerase reaction-restriction fragment length polymorphisms (RFLP) technique. Results: For the LPL-Hind IIIpolymorphism H+H+ genotype group, the triglycerides TG and very-low-density lipoprotein cholesterol VLDL-C concentrations were significantly higher and the high-density lipoprotein cholesterol HDL-C concentration was significantly lower than those of the H-H-genotype. ForAPO CII-Ava II polymorphisms, compared with those of the A2A2 genotype group, the total cholesterol TC, TG, low-density lipoprotein cholesterol LDL-C and VLDL-C concentrations were significantly increased in the A1A2 genotype group, while the HDL-C concentration was significantly decreased. Conclusions: The study revealed that the H+H+ or H +H-genotype of the LPL-Hind III polymorphism and the A1A1or A1A2 genotype of the APOCII-Ava II polymorphism were at higher risk of developing dysli-pidaemia compared to the H -H-genotype of the LPL-Hind III polymorphism and A2A2 genotype of the APOCII-Ava II polymorphism. (C) 2021 Cardiological Society of India. Published by Elsevier B.V.

Automated summary

This study investigated the relationship between smoking duration and the genetic polymorphisms of lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) in relation to dyslipidaemia. The results showed that individuals with the H+H+ or H+H genotype of the LPL-Hind III polymorphism and the A1A1 or A1A2 genotype of the APOCII-Ava II polymorphism were at a higher risk of developing dyslipidaemia.