Skoczynska Anna, Dobosz Tadeusz, Poreba Rafal, Turczyn Barbara, Derkacz Arkadiusz, Zoledziewska Magdalena, Jonkisz Anna, Lebioda Arleta
Department of Internal Medicine, Occupational Diseases and Hypertension, Wroclaw Medical University, L. Pasteur 4, 50-367 Wroclaw, Poland.
Eur J Intern Med. 2005 Nov;16(7):501-6. doi: 10.1016/j.ejim.2005.04.012.
The association between L162V polymorphism in the gene for peroxisome proliferator activated receptor (PPAR) alpha and the development of coronary heart disease was examined.
PPAR-alpha polymorphism was determined in 48 men with angiographically confirmed coronary atherosclerosis and in 51 healthy men.
The frequency of the V allele of the L162V polymorphism was four times higher in men with atherosclerosis (0.25 in studied group and 0.06 in controls). The polymorphism was not associated with changes in body mass index, lipid pattern, serum adhesion molecules, or vasoactive agents concentrations. The effect of the polymorphism on the serum interleukin-6 level (IL-6) was observed (p<0.01). The serum IL-6 level was higher in homozygotic than in heterozygotic subjects (p<0.02). Multivariate regression analysis showed the existence of a relationship between simvastatin therapy and serum IL-6 level (r=0.83; p<0.05) in the homozygotic men. While in homozygotic patients with atherosclerosis a negative linear correlation between serum IL-6 and NO concentration was shown, in heterozygotic men positive correlations between IL-6 or HDL cholesterol and adhesion molecule levels were found.
L162V polymorphism in the gene for PPAR-alpha seems to be associated with atherosclerosis through a mechanism including regulation of the IL-6 level.
研究了过氧化物酶体增殖物激活受体(PPAR)α基因中的L162V多态性与冠心病发生之间的关联。
对48例经血管造影证实患有冠状动脉粥样硬化的男性和51例健康男性进行了PPAR-α多态性检测。
动脉粥样硬化男性中L162V多态性的V等位基因频率比对照组高4倍(研究组为0.25,对照组为0.06)。该多态性与体重指数、血脂模式、血清黏附分子或血管活性物质浓度的变化无关。观察到该多态性对血清白细胞介素-6水平(IL-6)有影响(p<0.01)。纯合子受试者的血清IL-6水平高于杂合子受试者(p<0.02)。多变量回归分析显示,在纯合子男性中,辛伐他汀治疗与血清IL-6水平之间存在关联(r=0.83;p<0.05)。在患有动脉粥样硬化的纯合子患者中,血清IL-6与NO浓度呈负线性相关,而在杂合子男性中,发现IL-6或高密度脂蛋白胆固醇与黏附分子水平呈正相关。
PPAR-α基因中的L162V多态性似乎通过包括调节IL-6水平在内的机制与动脉粥样硬化相关。