Boes Eva, Kollerits Barbara, Heid Iris M, Hunt Steven C, Pichler Michaela, Paulweber Bernhard, Coassin Stefan, Adams Ted D, Hopkins Paul N, Lingenhel Arno, Wagner Stefanie A, Kronenberg Florian
Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Innsbruck, Austria.
Obesity (Silver Spring). 2008 Apr;16(4):827-33. doi: 10.1038/oby.2007.132. Epub 2008 Jan 31.
A previous epidemiological study showed an association of the insulin-induced gene 2 (INSIG2) gene with BMI. Additionally, experimental investigations in animals and cell culture provided evidence that this gene might be involved in lipoprotein and free fatty acid (FFA) metabolism. Therefore, the aim of this study was to examine the association between the rs7566605 variant near the INSIG2 gene and BMI and to extend it to other quantitative measures of obesity, as well as parameters of lipoprotein and FFA metabolism.
We genotyped rs7566605 in a group of severely obese white patients (n = 1,026) with an average BMI of 46.0 kg/m(2) and a control group (n = 818) from Utah, as well as in the Salzburg Atherosclerosis Prevention Program in Subjects at High Individual Risk (SAPHIR) study from Austria, which is based on a healthy working population (n = 1,696).
We observed no difference in the genotype frequency of rs7566605 of INSIG2 between obese subjects and population-based controls from Utah. Furthermore, we did not find evidence of an association with measures of body composition (BMI, waist, waist-to-hip ratio, percentage body fat, amount of visceral and subcutaneous abdominal adipose fat) or lipoprotein metabolism (total cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, triglycerides, and FFAs) in the Utah study population or in the independent SAPHIR study.
Our results do not support an association of the INSIG2 gene with the regulation of body weight or parameters related to lipoprotein metabolism.
先前的一项流行病学研究表明胰岛素诱导基因2（INSIG2）与体重指数（BMI）之间存在关联。此外，动物实验和细胞培养研究提供了证据，表明该基因可能参与脂蛋白和游离脂肪酸（FFA）代谢。因此，本研究的目的是检验INSIG2基因附近的rs7566605变异与BMI之间的关联，并将其扩展到肥胖的其他定量指标以及脂蛋白和FFA代谢参数。
我们对一组平均BMI为46.0kg/m²的重度肥胖白人患者（n = 1026）和来自犹他州的对照组（n = 818）中的rs7566605进行基因分型，同时也在奥地利的萨尔茨堡高危个体动脉粥样硬化预防项目（SAPHIR）研究中进行了基因分型，该研究基于健康工作人群（n = 1696）。
我们观察到肥胖受试者与犹他州基于人群的对照组之间INSIG2基因的rs7566605基因型频率没有差异。此外，在犹他州研究人群或独立的SAPHIR研究中，我们没有发现该基因与身体成分测量指标（BMI、腰围、腰臀比、体脂百分比、腹部内脏和皮下脂肪量）或脂蛋白代谢指标（总胆固醇、低密度脂蛋白（LDL）和高密度脂蛋白（HDL）胆固醇、甘油三酯和FFA）存在关联的证据。
我们的结果不支持INSIG2基因与体重调节或脂蛋白代谢相关参数之间存在关联。
