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首页> 外文期刊>Hormone and Metabolic Research >The - 11391 G/A polymorphism of the adiponectin gene promoter is associated with metabolic syndrome traits and the outcome of an energy-restricted diet in obese subjects.
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The - 11391 G/A polymorphism of the adiponectin gene promoter is associated with metabolic syndrome traits and the outcome of an energy-restricted diet in obese subjects.

机译:脂联素基因启动子的-11391 G / A多态性与代谢综合征特征以及肥胖受试者饮食受限的能量的结果有关。

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Adiponectin is an adipose tissue-specific hormone that is commonly decreased in obese subjects. Furthermore, single-nucleotide polymorphisms (SNPs) of the adiponectin gene have been associated with metabolic phenotypes. The present study investigated whether the adiponectin gene promoter variant -11391 G/A (rs17300539) could predict the risk of developing traits characterizing the metabolic syndrome (MetS) and the impact of weight management. The -11391 G/A SNP was genotyped in 180 Spanish volunteers (BMI: 31.4+/-3.2 kg/m (2); age: 35+/-5 years). Clinical measurements were determined at baseline, following an 8-week low-calorie diet (LCD), and at 32 and 60 weeks. At baseline, the GG genotype was associated with higher HOMA-IR, insulin and triacylglyceride concentrations than other genotypes (p<0.05) and was also related with a higher risk of insulin resistance (OR: 2.437, p=0.025) and MetS clinical manifestations (OR: 3.236, p=0.003). Following the LCD, the increased risk in GG subjects compared with others disappeared (p>0.05). By 32 weeks after dietary therapy (n=84), GG carriers had recovered the risk of metabolic comorbidities (OR: 2.420, p=0.043). This risk was even more evident after 60 weeks (OR: 2.875, p=0.014). These data show an increased risk of insulin resistance and MetS complications in obese subjects of the -11391 GG genotype. The risk was markedly reduced during an energy-restricted diet, but was not sustained. Carriage of the A allele therefore confers protection from weight regain, and the effect is particularly evident 32-60 weeks after the dietary intervention, when improvement in GG subjects had disappeared.
机译:脂联素是一种脂肪组织特异性激素,在肥胖受试者中通常会降低。此外,脂联素基因的单核苷酸多态性(SNP)已与代谢表型相关联。本研究调查了脂联素基因启动子变体-11391 G / A(rs17300539)是否可以预测发展表征代谢综合征(MetS)的性状的风险以及体重管理的影响。 -11391 G / A SNP在180名西班牙志愿者中进行了基因分型(BMI:31.4 +/- 3.2 kg / m(2);年龄:35 +/- 5岁)。临床测量是在基线,8周低热量饮食(LCD)之后以及32和60周时确定的。在基线时,GG基因型与其他基因型相关的HOMA-IR,胰岛素和甘油三酯浓度较高(p <0.05),并且与胰岛素抵抗的风险较高(OR:2.437,p = 0.025)和MetS临床表现有关(OR:3.236,p = 0.003)。在LCD之后,GG受试者与其他受试者相比增加的风险消失了(p> 0.05)。饮食治疗后32周(n = 84),GG携带者已恢复了代谢合并症的风险(OR:2.420,p = 0.043)。 60周后,这种风险更加明显(或:2.875,p = 0.014)。这些数据表明,在-11391 GG基因型肥胖的受试者中,胰岛素抵抗和MetS并发症的风险增加。在能量限制饮食中,该风险明显降低,但并没有持续。因此,A等位基因的携带赋予了防止体重恢复的保护,当GG受试者的症状消失时,饮食干预后32-60周的效果尤为明显。

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