[Association between lipoprotein lipase hind III polymorphism and serum levels of lipids in Semnan City]

Lipoprotein lipase [LPL] is one of the key enzymes regulating the metabolism of triglycerides [TG] and HDL cholesterol. The lipoprotein lipase [LPL] gene polymorphisms are possibly involved in the pathophysiology of dyslipidemia. Hind III polymorphism is one of the most common polymorphisms in LPL gene. In some studies, association of Hind III polymorphism with dyslipidemia has been reported. Due to the high incidence of dyslipidemia in Iranian adults, this study was designed to investigate the frequency of rare allele [H-] LPL gene Hind III polymorphism and its association with serum lipids levels in an Iranian population, Total genomic DNA was prepared from 76 Iranian patients with hyperlipidemia [Total cholesterol [TC]>200 mg/dl, Triglyceride [TG]>150 mg/dl] and 75 healthy subjects [TC<200 mg/dl, TG<150]. The Hind III polymorphism was analyzed by polymerase chain reaction and restriction fragment length polymorphism. The frequencies of the Hind III polymorphism minor allele [H-] were 17 and 30 in the case and control groups respectively [P<0.01]. In the case group, patients with H+H+genotype had significantly higher mean total cholesterol [TC] and low density lipoprotein [LDL], compared to those with H+H-and H-H-genotypes [P<0.05]. The presence of rare H+allele was associated with increased TC and LDL-c levels in the studied population. The association between the LPL gene Hind III polymorphism and dyslipidemia is quite complicated and genotyping of LPL Hind III polymorphism in a larger-scale screening and with other polymorphisms is necessary and justifiable

Study of XmnI polymorphism in 5 region of the apoAl gene in Iranian hyperlipidemic subjects

Several studies have demonstrated the relationship between polymorphisms in the ApoAl - CIH - AIV gene cluster and hyperlipidemia. This study was conducted to elucidate the association between polymorphism of ApoAI/XmnI and Iranian hyperlipidemic subjects. Total genomic DNA was prepared from seventy-six Iranian patient with primary hyperlipidemia and seventy-five normolipidemic subjects. The subjects in the control group were age-and sex-matched to the patients. Fragment of 392 bp for 5 region of the apoAl gene [C-2500T] was amplified by polymerase chain reaction [PCR]. In the hyperlipidemic group, the genotype frequency of X1X1, X1X2, X2X2 were 0.63, 0.24, 0.13, respectively. In the control group those were 0.81, 0.11 and 0.08, respectivley. There was a significant difference [p<0.05] between 2 groups. The rare allele [X2] was more frequent in hyperlipidemic group than in controls [p<0.01]. Various genotypes of apoAl/Xmnl had no significant effect on lipids or apoAI levels in hyperlipidemic group. The above results show that polymorphism ApoAl/XmnI is associated with hyperlipidemia in Iranian hyperlipidemic subjects. Therefore, our data confirmed the previously reported association between genetic polymorphism ApoAI/XmnI and hyperlipidemia