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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inflammation and adipose tissue macrophages in lipodystrophic mice
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Inflammation and adipose tissue macrophages in lipodystrophic mice

机译：脂肪营养不良小鼠的炎症和脂肪组织巨噬细胞

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摘要

Lipodystrophy and obesity are opposites in terms of a deficiency versus excess of adipose tissue mass, yet these conditions are accompanied by similar metabolic consequences, including insulin resistance, dyslipidemia, hepatic steatosis, and increased risk for diabetes and atherosclerosis. Hepatic and myocellularsteatosis likely contribute to metabolic dysregulation in both states. Inflammation and macrophage infiltration into adipose tissue also appear to participate in the pathogenesis of obesity-induced insulin resistance, but their contributions to lipodystrophy-induced insulin resistance have not been evaluated. We used aP2-nSREBP-1c transgenic (Tg) mice, an established model of lipodystrophy, to ask this question. Circulating cytokine elevations suggested systemic inflammation but even more dramatic was the number of infiltrating macrophages in all white and brown adipose tissue depots of the Tg mice; in contrast, there was no evidence of inflammatory infiltrates or responses in any other tissue including liver. Despite there being overt evidence of adipose tissue inflammation, antiinflammatory strategies including salicylate treatment and genetic suppression of myeloid NF-κB signaling that correct insulin resistance in obesity were ineffective in the lipodystrophic mice. We further showed that adipose tissue macrophages (ATMs) in lipodystrophy and obesity are very different in terms of activation state, gene expression patterns, and response to lipopolysaccharide. Although ATMs are even more abundant in lipodystrophy than in obesity, they have distinct phenotypes and likely roles in tissue remodeling, but do not appear to be involved in the pathogenesis of insulin resistance.
机译：脂肪营养不良和肥胖在脂肪组织量不足与过量方面是相反的，但是这些状况伴随着类似的代谢后果，包括胰岛素抵抗，血脂异常，肝脂肪变性以及糖尿病和动脉粥样硬化的风险增加。在这两种状态下，肝脂肪变性和肌细胞脂肪变性都可能导致代谢异常。炎症和巨噬细胞浸润到脂肪组织中似乎也参与了肥胖诱导的胰岛素抵抗的发病机理，但是尚未评估它们对脂肪营养不良诱导的胰岛素抵抗的贡献。我们使用aP2-nSREBP-1c转基因（Tg）小鼠（脂肪营养不良的已建立模型）来问这个问题。循环中的细胞因子升高提示系统性炎症，但更为显着的是Tg小鼠所有白色和棕色脂肪组织贮库中浸润性巨噬细胞的数量。相反，在包括肝脏在内的任何其他组织中都没有炎症浸润或反应的证据。尽管有明显的脂肪组织炎症的证据，但在肥胖性营养不良的小鼠中，包括水杨酸盐治疗和对抑制肥胖症中的胰岛素抵抗的髓样NF-κB信号的遗传抑制等抗炎策略无效。我们进一步表明，脂肪营养不良和肥胖症中的脂肪组织巨噬细胞（ATM）在激活状态，基因表达模式和对脂多糖的反应方面都存在很大差异。尽管ATM在脂肪营养不良中比在肥胖症中更为丰富，但它们具有独特的表型，并可能在组织重塑中发挥作用，但似乎不参与胰岛素抵抗的发病机理。

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  • 作者

    Laura Herrero; Hagit Shapiro; Ali Nayer; Jongsoon Lee; Steven E. Shoelson;

  • 作者单位

    Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02115 Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Barcelona, Barcelona, Spain;

    Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02115;

    Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02115;

    Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02115;

    Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02115;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    diabetes; insulin resistance; obesity;

    机译：糖尿病;胰岛素抵抗;肥胖;

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