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Inflammation Might Help Defeat Diabetes

机译:炎症可能有助于战胜糖尿病

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With the rise in obesity has come a corresponding increase in rates of type 2 diabetes, in which fat and muscle cells become resistant to insulin, the hormone that transports energy-rich glucose into them. The health implications of diabetes are daunting-heart disease, nerve damage, and worse-so the search for a cure has been fierce. Yet many scientists may have missed a crucial clue by focusing on the wrong root cause of the disease. Researchers have long tied type 2 diabetes to chronic inflammation, caused by a ramping-up of immune system activity that ultimately damages insulin receptor signalling and leads to insulin resistance. But in September, Umut Ozcan, an obesity researcher at Children's Hospital Boston, reported that a key inflammatory protein actually reduces insulin resistance in obese diabetic mice, curing them of diabetes. The protein, called xbp-is, turns on genes that direct the assembly of other proteins that keep insulin function working correctly in the cells. Ozcan realized that inflammation might help when he noticed that in obese diabetic mice, xbp-is failed to enter the cell nucleus, where insulin function is regulated. By comparing the behavior of xbp-is in the obese mice with that in lean, healthy ones, he discovered an inflammatory protein that modifies xbp-is in healthy animals so it can be shuttled into the nucleus.
机译:随着肥胖的增加,2型糖尿病的发病率也相应增加,其中脂肪和肌肉细胞对胰岛素具有抵抗力,胰岛素是一种将能量丰富的葡萄糖转运到其中的激素。糖尿病对健康的影响是令人生畏的心脏病,神经损伤和病情恶化,因此,寻找治疗方法的工作非常激烈。然而,许多科学家通过关注疾病的错误根源可能错过了关键线索。长期以来,研究人员将2型糖尿病与慢性炎症联系在一起,这种慢性炎症是由于免疫系统活性的增强而引起的,最终导致胰岛素受体信号传导受损并导致胰岛素抵抗。但是在9月,波士顿儿童医院肥胖研究人员Umut Ozcan报告说,一种关键的炎症蛋白实际上降低了肥胖糖尿病小鼠的胰岛素抵抗,从而治愈了糖尿病。这种叫做xbp-is的蛋白质打开了指导其他蛋白质组装的基因,这些蛋白质使胰岛素功能在细胞中正常工作。 Ozcan意识到,在肥胖的糖尿病小鼠中,xbp-未能进入调节胰岛素功能的细胞核时,炎症可能会有所帮助。通过比较肥胖小鼠与瘦弱健康小鼠的xbp-is行为,他发现了一种可以改变健康动物中xbp-is的炎症蛋白,因此可以将其穿梭到细胞核中。

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  • 来源
    《Discover》 |2012年第1期|p.79|共1页
  • 作者

    MELINDA WENNER MOYER;

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