A Promoter Genotype and Oxidative Stress Potentially Link Resistin to Human Insulin Resistance
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- Steve R. Smith
- Pennington Biomedical Research Center, Baton Rouge, Louisiana
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- Fulu Bai
- Pennington Biomedical Research Center, Baton Rouge, Louisiana
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- Chantal Charbonneau
- Pennington Biomedical Research Center, Baton Rouge, Louisiana
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- Lenka Janderová
- Pennington Biomedical Research Center, Baton Rouge, Louisiana
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- George Argyropoulos
- Pennington Biomedical Research Center, Baton Rouge, Louisiana
書誌事項
- 公開日
- 2003-07-01
- DOI
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- 10.2337/diabetes.52.7.1611
- 公開者
- American Diabetes Association
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説明
<jats:p>Insulin resistance is a component of type 2 diabetes and often precedes pancreatic β-cell failure. Contributing factors include obesity and a central pattern of fat accumulation with a strong genetic component. The adipocyte secreted hormone resistin has been proposed as a link between the adipocyte and insulin resistance by inhibition of insulin-stimulated glucose uptake and/or blocking adipocyte differentiation. Here we report that the G/G genotype of a single nucleotide polymorphism (SNP) in the promoter of the human resistin gene, −180C>G, had significantly increased basal promoter activity in adipocytes. These data were recapitulated in vivo, where G/G homozygotes had significantly higher resistin mRNA levels in human abdominal subcutaneous fat. A significant interaction was also found between the −180C>G SNP, a marker of oxidative stress (NAD[P]H quinone oxidoreductase mRNA) and homeostasis model assessment of insulin resistance. In addition, resistin mRNA was positively and independently correlated with insulin resistance and hepatic fat as measured by liver X-ray attenuation. These data implicate resistin in the pathophysiology of the human insulin resistance syndrome, an effect mediated by the −180C>G promoter SNP and potentially cellular oxidative stress.</jats:p>
収録刊行物
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- Diabetes
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Diabetes 52 (7), 1611-1618, 2003-07-01
American Diabetes Association
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詳細情報 詳細情報について
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- CRID
- 1360011144043750400
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- NII論文ID
- 30026269301
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- ISSN
- 1939327X
- 00121797
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- データソース種別
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- Crossref
- CiNii Articles

