Department of Molecular Medicine, Institute of Experimental Medicine, Istanbul University, Capa-Istanbul, Turkey.
In Vivo. 2011 May-Jun;25(3):425-30.
Obesity is a multifactorial, chronic disorder leading to adverse metabolic effects on plasma lipid levels. Apolipoprotein AI (Apo AI) is the major structural component of high-density lipoprotein (HDL) and is involved in the esterification of cholesterol as a cofactor of lecithin-cholesterol acyltransferase (LCAT) and thus plays a major role in cholesterol efflux from peripheral cells. The APOA1 gene is associated with changes in lipid metabolism. A common gene polymorphism described in the APOA1 promoter region consists of the exchange of guanine (G) for adenine (A) at a position -75 bp upstream of the transcription origin. The relationship between lipid levels in obese children and the APOA1 MspI polymorphisms, was examined.
Three separate groups were included, the patient group of obese children with hyperlipidemia; the obese control group (control group I) consisted of obese children without hyperlipidemia; and the healthy control group (control group II) contained healthy children with neither hyperlipidemia nor obesity. The related gene segments were amplified by polymerase chain reaction and determined different patterns were determined using denaturating gradient gel electrophoresis and positive results were confirmed automatic sequence analysis. All the results were analyzed by Proseq and BioEdit computer programmes.
The A allele was found to be more frequent in control group I compared to the patient group (p=0.035). Very low-density lipoprotein (VLDL), LDL and triglyceride (TG), levels were statistically higher in the patients carrying the GA genotype than in control group I, and body mass index (BMI), VLDL and TG levels were statistically higher than in control group II (p<0.05). There was no relationship between -75(G/A) polymorphism and serum lipid HDL-cholesterol levels when patient values were compared to those of the controls (p>0.05). Additionally, according to the -75 GA genotypes, those in control group I with the GA genotype had elevated total cholesterol levels compared to those with the GG genotype (p<0.010). In conclusion, carrying the A allele could confer a higher risk of hyperlipidemia in obese children.
肥胖是一种多因素、慢性疾病，会导致血浆脂质水平的代谢不良。载脂蛋白 AI（Apo AI）是高密度脂蛋白（HDL）的主要结构成分，作为卵磷脂-胆固醇酰基转移酶（LCAT）的辅助因子参与胆固醇酯化，因此在胆固醇从外周细胞流出中起主要作用。APOA1 基因与脂质代谢变化有关。APOA1 启动子区域描述的一种常见基因多态性由鸟嘌呤（G）到腺嘌呤（A）的交换组成，位于转录起始点上游的-75bp 位置。研究了肥胖儿童的血脂水平与 APOA1 MspI 多态性的关系。
纳入了三组，患者组为患有高脂血症的肥胖儿童；肥胖对照组（对照组 I）由无高脂血症的肥胖儿童组成；健康对照组（对照组 II）由既无高脂血症也无肥胖的健康儿童组成。通过聚合酶链反应扩增相关基因片段，采用变性梯度凝胶电泳确定不同的模式，并通过自动序列分析确认阳性结果。所有结果均通过 Proseq 和 BioEdit 计算机程序进行分析。
发现与患者组相比，对照组 I 中 A 等位基因更为常见（p=0.035）。携带 GA 基因型的患者极低密度脂蛋白（VLDL）、LDL 和甘油三酯（TG）水平明显高于对照组 I，体重指数（BMI）、VLDL 和 TG 水平明显高于对照组 II（p<0.05）。与对照组相比，患者的-75（G/A）多态性与血清脂质 HDL-胆固醇水平之间无关系（p>0.05）。此外，根据-75GA 基因型，对照组 I 中携带 GA 基因型的个体总胆固醇水平高于携带 GG 基因型的个体（p<0.010）。结论：携带 A 等位基因可能使肥胖儿童患高脂血症的风险增加。
