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Neutralization of Osteopontin Inhibits Obesity-Induced Inflammation and Insulin Resistance

机译：中和骨桥蛋白抑制肥胖引起的炎症和胰岛素抵抗

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摘要

Obesity is associated with a state of chronic low-grade inflammation mediated by immune cells that are primarily located to adipose tissue and liver. The chronic inflammatory response appears to underlie obesity-induced metabolic deterioration including insulin resistance and type 2 diabetes. Osteopontin (OPN) is an inflammatory cytokine, the expression of which is strongly upregulated in adipose tissue and liver upon obesity. Here, we studied OPN effects in obesity-induced inflammation and insulin resistance by targeting OPN action in vivo.
机译：肥胖与主要位于脂肪组织和肝脏的免疫细胞介导的慢性低度炎症状态有关。慢性炎症反应似乎是肥胖引起的代谢恶化的基础，包括胰岛素抵抗和2型糖尿病。骨桥蛋白（OPN）是一种炎症性细胞因子，肥胖时其表达在脂肪组织和肝脏中强烈上调。在这里，我们通过针对体内OPN作用研究了OPN在肥胖引起的炎症和胰岛素抵抗中的作用。

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  • 来源
    《Diabetes》 |2010年第4期|p.935-946|共12页
  • 作者

    Florian W Kiefer Maximilian Zeyda Karina Gollinger Birgit Pfau Angelika Neuhofer Thomas Weichhart Marcus D Säemann René Geyeregger Michaela Schlederer Lukas Kenner Thomas M Stulnig;

  • 作者单位

    Florian W. Kiefer,1 Maximilian Zeyda,1 Karina Gollinger,1 Birgit Pfau,1 Angelika Neuhofer,1 Thomas Weichhart,2 Marcus D. Säemann,2 René Geyeregger,1 Michaela Schlederer,3 Lukas Kenner,3'4 and Thomas M. Stulnig1From the 1 Clinical Division of Endocrinology and Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria, the 2 Clinical Division of Nephrology and Dialysis, Department of Medicine UI, Medical University of Vienna, Vienna, Austria, the 3 Ludwig Boltzmann Institute for Cancer Research, Medical University of Vienna, Vienna, Austria, and the 4 Department of Pathology, Medical University of Vienna, Vienna, AustriaCorresponding author Thomas M. Stulnig, thomas.stulnig@meduniwien.ac.at.Received 17 March 2009 and accepted 17 January 2010. Published ahead of print at http://diabetes.diabetesjaurnals.org on 27 January 2010. DOI: 10.2337/db09-0404.© 2010 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by -nc-nd/3.0/ for details.The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C Section 1734 solely to indicate this fact.,;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
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  • 入库时间 2022-08-17 13:45:41

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