ADAM17_i33708A>G polymorphism interacts with dietary n-6 polyunsaturated fatty acids to modulate obesity risk in the Genetics of Lipid Lowering Drugs and Diet Network study.
ADAM17_i33708A>G polymorphism interacts with dietary n-6 polyunsaturated fatty acids to modulate obesity risk in the Genetics of Lipid Lowering Drugs and Diet Network study.
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DOI：
10.1016/j.numecd.2009.06.011
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发表时间：
2010-12
期刊：
影响因子：
--
通讯作者：
Ordovás JM
中科院分区：
文献类型：
--
作者：
Junyent M;Parnell LD;Lai CQ;Arnett DK;Tsai MY;Kabagambe EK;Straka RJ;Province M;An P;Smith CE;Lee YC;Borecki I;Ordovás JM
解整合素和金属蛋白酶 ADAM17，也称为肿瘤坏死因子 α 转换酶，在脂肪细胞中表达。重要的是，ADAM17 表达水平升高与肥胖和胰岛素抵抗有关。因此，本研究的目的是评估六个 ADAM17 单核苷酸多态性 (SNP)（m1254A>G、i14121C>A、i33708A>G、i48827A>C、i53440C>T 和 i62781G>T）与胰岛素抵抗表型和肥胖风险的关联，以及它们与膳食多不饱和脂肪酸的潜在相互作用（多不饱和脂肪酸）。对参加降脂药物和饮食遗传学网络 (GOLDN) 研究的 936 名受试者（448 名男性/488 名女性）进行了 ADAM17 SNP 基因分型。人体测量和生化测量通过标准程序确定。使用经过验证的调查问卷估算 PUFA 摄入量。 ADAM17_m1254A>G 多态性的 G 等位基因携带者与 AA 受试者相比，肥胖风险显着更高 (P=0.003)、个子更矮 (P=0.017)、胰岛素水平更高 (P=0.016) 和 HDL-C 浓度更低 (P=0.027)。对于 ADAM17_i33708A>G SNP，A 等位基因纯合子比 GG 受试者显示出更高的肥胖风险 (P=0.001)、更重 (P=0.011)、更高的 BMI (P=0.005) 和更高的腰围测量值 (P=0.023)。发现了显着的基因-饮食相互作用 (P=0.030)，其中在 (n-6) PUFA 摄入量低的受试者中观察到 i33708A 等位基因与肥胖的有害关联 (P<0.001)，而在 (n-6) PUFA 摄入量高的受试者中肥胖风险没有差异 (P>0.5) 这些发现支持 ADAM17 (m1254A>G 和i33708A>G) SNP 可能会增加肥胖风险。对于 ADAM17_i33708A>G SNP，这种风险可能会通过 (n-6) PUFA 摄入量进一步调节。
The disintegrin and metalloproteinase ADAM17, also known as tumor necrosis factor alpha converting enzyme, is expressed in adipocytes. Importantly, elevated levels of ADAM17 expression have been linked to obesity and insulin resistance. Therefore, the aim of this study was to evaluate the association of six ADAM17 single nucleotide polymorphisms (SNPs) (m1254A>G, i14121C>A, i33708A>G, i48827A>C, i53440C>T, and i62781G>T) with insulin-resistance phenotypes and obesity risk, and their potential interactions with dietary polyunsaturated fatty acids (PUFA). ADAM17 SNPs were genotyped in 936 subjects (448 men/488 women) who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. Anthropometrical and biochemical measurements were determined by standard procedures. PUFA intake was estimated using a validated questionnaire. G allele carriers at the ADAM17_m1254A>G polymorphism exhibited significantly higher risk of obesity (P=0.003), were shorter (P=0.017), had higher insulin (P=0.016), and lower HDL-C concentrations (P=0.027) than AA subjects. For the ADAM17_i33708A>G SNP, homozygotes for the A allele displayed higher risk of obesity (P=0.001), were heavier (P=0.011), had higher BMI (P=0.005), and higher waist measurements (P=0.023) than GG subjects. A significant gene-diet interaction was found (P=0.030), in which the deleterious association of the i33708A allele with obesity was observed in subjects with low intakes from (n-6) PUFA (P<0.001), whereas no differences in obesity risk were seen among subjects with high (n-6) PUFA intake (P>0.5) These findings support that ADAM17 (m1254A>G and i33708A>G) SNPs may contribute to obesity risk. For the ADAM17_i33708A>G SNP, this risk may be further modulated by (n-6) PUFA intake.
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影响因子：
4.9
作者：
Brand, E;Schorr, U;Sharma, AM
通讯作者：
Sharma, AM
DOI：
10.1038/oby.2005.263
发表时间：
2005-12-01
期刊：
OBESITY RESEARCH
影响因子：
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作者：
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作者：
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影响因子：
8.2
作者：
Ramel, A.;Martinez, A.;Thorsdottir, I.
通讯作者：
Thorsdottir, I.
DOI：
10.1016/s0167-4781(02)00589-4
发表时间：
2003-01-03
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
影响因子：
--
作者：
Voros, G;Maquoi, E;Lijnen, HR
通讯作者：
Lijnen, HR