Boumaiza Imen, Omezzine Asma, Rejeb Jihène, Rebhi Lamia, Ouedrani Amani, Ben Rejeb Nabila, Nabli Naoufel, Ben Abdelaziz Ahmed, Bouslama Ali
Department of Biochemistry, UR MSP 28/04, Sahloul University Hospital, Sousse, Tunisia.
Genet Test Mol Biomarkers. 2012 Jul;16(7):726-33. doi: 10.1089/gtmb.2011.0324. Epub 2012 Jun 26.
Leptin is a key hormone of weight regulation that modulates food intake. Since the elaboration of the leptin action mechanism, several studies tried to establish the relationship between obesity and the common polymorphisms of leptin (LEP) and leptin receptor (LEPR) genes, but results were controversial. We studied the association of G2548A of the LEP gene and Q223R of LEPR gene polymorphisms with obesity and metabolic syndrome (MetS). We recruited 169 nonobese volunteers (body mass index [BMI] < 30 kg/m(2)) and 160 obese ones (BMI ≥ 30 kg/m(2)). Glucose, insulin, and lipids were measured. BMI, homeostasis model assessment-insulin resistance (HOMA-IR), and daily energy intake were calculated. After adjustment to confounders parameters, 2548AA was found to increase the MetS (p=0.043) and obesity risk (p=0.019) in the studied population. After stratification according to the degree of obesity, the odds ratio [OR] of 2548AA was associated with moderate obesity (p=0.048) and morbid obesity (p=0.048). The LEPR 223RR genotype was associated with obesity in the studied population (OR=1.74, p=0.037) and only in the overweight (OR=1.8, p=0.049). Subjects with 2548AA had significantly higher BMI, daily energy intake, total cholesterol (TC), waist circumference (WC), insulinemia, and low high-density lipoprotein-cholesterol (HDL-C) levels. With regard to 223RR, we noted a significantly higher daily energy intake, BMI, TC, glycemia, insulinemia, HOMA-IR index, and low HDL-C levels. Haplotype model AR (2548A+223R) and AQ (2548A+223Q) increased the risk of obesity (OR=3.36, p<0.001; OR=2.56, p=0.010, respectively). When we added daily energy intake in adjustment, these significant associations disappeared. In addition, the AR and AQ increased the MetS risk. This significant association persisted after we had added daily energy intake in adjustment. This study showed that LEP G2548A and LEPR Q223R polymorphisms and haplotype combination were associated with MetS and obesity risk in Tunisian volunteers.
瘦素是体重调节的关键激素，可调节食物摄入量。自瘦素作用机制阐述以来，多项研究试图确立肥胖与瘦素（LEP）基因和瘦素受体（LEPR）基因常见多态性之间的关系，但结果存在争议。我们研究了LEP基因的G2548A和LEPR基因多态性的Q223R与肥胖和代谢综合征（MetS）的关联。我们招募了169名非肥胖志愿者（体重指数[BMI]<30kg/m²）和160名肥胖者（BMI≥30kg/m²）。测量了血糖、胰岛素和血脂。计算了BMI、稳态模型评估-胰岛素抵抗（HOMA-IR）和每日能量摄入量。在对混杂因素参数进行调整后，发现2548AA会增加研究人群中患MetS的风险（p=0.043）和肥胖风险（p=0.019）。根据肥胖程度分层后，2548AA的优势比[OR]与中度肥胖（p=0.048）和病态肥胖（p=0.048）相关。LEPR 223RR基因型与研究人群中的肥胖相关（OR=1.74，p=0.037），且仅与超重相关（OR=1.8，p=0.049）。携带2548AA的受试者的BMI、每日能量摄入量、总胆固醇（TC）、腰围（WC）、胰岛素血症和低高密度脂蛋白胆固醇（HDL-C）水平显著更高。关于223RR，我们注意到其每日能量摄入量、BMI、TC、血糖、胰岛素血症、HOMA-IR指数和低HDL-C水平显著更高。单倍型模型AR（2548A+223R）和AQ（2548A+223Q）增加了肥胖风险（分别为OR=3.36，p<0.001；OR=2.56，p=0.010）。当我们在调整中加入每日能量摄入量时，这些显著关联消失。此外，AR和AQ增加了患MetS的风险。在我们在调整中加入每日能量摄入量后，这种显著关联仍然存在。这项研究表明，LEP G2548A和LEPR Q223R多态性及单倍型组合与突尼斯志愿者的MetS和肥胖风险相关。
