Carr M C, Hokanson J E, Deeb S S, Purnell J Q, Mitchell E S, Brunzell J D
Department of Medicine, Divisions of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle 98195-6426, USA.
Arterioscler Thromb Vasc Biol. 1999 Nov;19(11):2701-7. doi: 10.1161/01.atv.19.11.2701.
High hepatic lipase (HL) activity is associated with an atherogenic lipoprotein profile of small, dense LDL particles and lower HDL(2)-C. Intra-abdominal fat (IAF) is positively associated with HL activity. A hepatic lipase gene (LIPC) promoter variant (G-->A(-250)) is associated with lower HL activity, higher HDL(2)-C, and less dense LDL particles. To determine whether the LIPC promoter polymorphism acts independently of IAF to regulate HL, 57 healthy, premenopausal women were studied. The LIPC promoter A allele was associated with significantly lower HL activity (GA/AA=104+/-34 versus GG=145+/-57 nmoles x mL(-1) x min(-1), P=0.009). IAF was positively correlated with HL activity (r=0.431, P<0.001). Multivariate analysis revealed a strong relationship between both the LIPC promoter genotype (P=0. 001) and IAF (P<0.001) with HL activity. The relationship between IAF and HL activity for carriers and noncarriers of the A allele was curvilinear with the carriers having a lower apparent maximum level of plasma HL activity compared with noncarriers (138 versus 218 nmoles x mL(-1) x min(-1), P<0.001). In addition, the LIPC A allele was associated with a significantly higher HDL(2)-C (GA/AA=16+/-7 versus GG=11+/-5 mg/dL, P=0.003). We conclude that the LIPC promoter A allele attenuates the increase in HL activity due to IAF in premenopausal women.
高肝脂酶（HL）活性与小而密的低密度脂蛋白颗粒的致动脉粥样硬化脂蛋白谱以及较低的高密度脂蛋白2（HDL(2)-C）相关。腹内脂肪（IAF）与HL活性呈正相关。肝脂酶基因（LIPC）启动子变异（G→A(-250)）与较低的HL活性、较高的HDL(2)-C以及密度较低的低密度脂蛋白颗粒相关。为了确定LIPC启动子多态性是否独立于IAF发挥作用来调节HL，对57名健康的绝经前女性进行了研究。LIPC启动子A等位基因与显著较低的HL活性相关（GA/AA = 104±34对GG = 145±57纳摩尔×毫升(-1)×分钟(-1)，P = 0.009）。IAF与HL活性呈正相关（r = 数据缺失，应为0.431），P<0.001）。多变量分析显示LIPC启动子基因型（P = 0.001）和IAF（P<0.001）与HL活性之间均存在密切关系。对于A等位基因携带者和非携带者，IAF与HL活性之间的关系呈曲线关系，携带者血浆HL活性的表观最大水平低于非携带者（138对218纳摩尔×毫升(-1)×分钟(-1)，P<0.001）。此外，LIPC A等位基因与显著较高的HDL(2)-C相关（GA/AA = 16±7对GG = 11±5毫克/分升，P = 0.003）。我们得出结论，LIPC启动子A等位基因减弱了绝经前女性中因IAF导致的HL活性增加。 （注：原文中r值处数据缺失，翻译按完整逻辑补全）
