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检测分析肥胖儿童脂蛋白脂酶(LPL)基因多态及其与脂代谢的关系。结果表明:肥胖组较对照组LPL Pvu Ⅱ酶切点+/+基因型频率显著升高(P<0.05);肥胖组Pvu Ⅱ+/+基因型者较-/-基因型者高密度脂蛋白胆固醇(HDL-c)水平显著降低(P<0.05);Hind Ⅲ+/+基因型者较-/-和+/-基因型者血TG、TC水平显著升高(P<0.05);有Ser~(447)-Stop突变者较无此突变者血低密度脂蛋白胆固醇(LDL-c)水平显著降低(P<0.05)、HDL-c水平显著升高(P<0.05)。提示肥胖儿童脂代谢异常有遗传倾向,LPL基因Pvu Ⅱ+/+、Hind Ⅲ+/+、无Ser~(447)-Stop突变基因型肥胖儿童较其它基因型者成人后患冠心病的危险性更大。
Detection and analysis of obesity children lipoprotein lipase (LPL) gene polymorphism and its relationship with lipid metabolism. The results showed that the frequencies of LPL Pvu Ⅱ cleavage site + / + genotypes in obesity group were significantly higher than those in control group (P <0.05), and those in Pvu Ⅱ + / + genotypes in obesity group were higher than those in control group (P <0.05). The levels of serum TG and TC in Hind Ⅲ + / + genotypes were significantly higher than those in the - / - and +/- genotypes (P <0.05) The levels of LDL-c and HDL-c in ~ (447) -Stop mutant were significantly lower than those without mutation (P <0.05). The results suggest that there is a genetic predisposition to fat metabolism abnormalities in obese children. The risk of coronary heart disease in adults with obesity is higher than that of other genotypes in obese children with LPL gene Pvu Ⅱ + / +, Hind Ⅲ + / +, without Ser ~ (447) -Stop mutation Big.