Mancini Francesco P, Sabatino Lina, Colantuoni Vittorio, Pasanisi Fabrizio, Finelli Carmine, Contaldo Franco, Masulli Maria, Riccardi Gabriele, Vaccaro Olga
Department of Biological and Environmental Sciences, University of Sannio, Benevento, Italy.
Clin Endocrinol (Oxf). 2003 Dec;59(6):817-22. doi: 10.1046/j.1365-2265.2003.01926.x.
To analyse the association of the UCP2 gene, alone or in combination with the PPARgamma2 gene, with obesity.
Cross-sectional, case-control study.
From a working population of 4500 Italian Caucasian employees of the Italian telephone company participating in a firm-sponsored health screening programme, we selected all those with obesity [n = 122; body mass index (BMI) > or = 30 kg/m2]. For each case, three nonobese age- and sex-matched individuals were selected as controls from the same population (n = 374). Included in the study were also 76 severely obese (BMI > or = 40 kg/m2) patients consecutively admitted to the obesity clinic of the department. Diabetic individuals were excluded.
The -866G/A UCP2 and the Pro12Ala PPARgamma2 polymorphisms were determined on genomic DNA of the studied individuals. Several metabolic and anthropometric measures were also obtained, like plasma glucose, insulin, triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol and BMI.
BMI, plasma glucose, insulin, triglycerides, total and HDL cholesterol were not significantly different in carriers and noncarriers of the -866G/A variant. No significant association was observed between the -866G/A UCP2 gene polymorphism and moderate or severe obesity. This was also observed when the UCP2 polymorphism was analysed in combination with the PPARgamma2 polymorphisms.
The -866G/A variants of the UCP2 gene are not associated with either obesity or other features of the metabolic syndrome in the studied groups of the Italian population. This negative finding is not modified after a combined analysis of the UCP2 polymorphism and the Pro12Ala polymorphism of PPARgamma2.
分析解偶联蛋白2(UCP2)基因单独或与过氧化物酶体增殖物激活受体γ2(PPARγ2)基因联合与肥胖的相关性。
横断面病例对照研究。
从参与公司赞助的健康筛查项目的4500名意大利白种裔意大利电话公司员工的工作人群中,我们选取了所有肥胖者[n = 122;体重指数(BMI)≥30 kg/m²]。对于每例患者,从同一人群中选取3名年龄和性别匹配的非肥胖个体作为对照(n = 374)。纳入研究的还包括76例连续入住该科室肥胖门诊的重度肥胖患者(BMI≥40 kg/m²)。排除糖尿病患者。
在研究对象的基因组DNA上测定UCP2基因-866G/A和PPARγ2基因Pro12Ala多态性。还获取了多项代谢和人体测量指标,如血糖、胰岛素、甘油三酯、总胆固醇、高密度脂蛋白(HDL)胆固醇和BMI。
-866G/A变异携带者和非携带者的BMI、血糖、胰岛素、甘油三酯、总胆固醇和HDL胆固醇无显著差异。未观察到-866G/A UCP2基因多态性与中度或重度肥胖之间存在显著关联。当联合分析UCP2多态性与PPARγ2多态性时,也观察到同样结果。
在意大利人群的研究组中,UCP2基因的-866G/A变异与肥胖或代谢综合征的其他特征均无关联。在联合分析UCP2多态性和PPARγ2基因Pro12Ala多态性后,这一阴性结果未改变。