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In This Issue of Diabetes

机译:在本期糖尿病

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Muscle stem cells, or satellite cells, are likely impaired in type 1 diabetes and as such may contribute to the skeletal muscle atrophy that is often observed as a complication of the disease. This is according to the outcome of a study by D'Souza et al. (p. 3053) in which they investigated the condition of satellite cells in mice with type 1 diabetes and, significantly, human muscle biopsy samples obtained from young adult donors with the disease. According to the authors, mice that naturally develop type 1 diabetes at 4 weeks (Akita mice) had reduced endurance and increased muscle damage following exercise in comparison to controls. An examination of satellite cells in the two groups revealed a more general failure to generate new muscle cells (myogenesis) in the mice with diabetes, and consequently satellite cell content was also reduced. Additional markers of myogenesis were also reduced in the diabetic mice. To then understand the potential pathways involved, the authors investigated Notch signaling on the basis of its well-established role in myogenesis. Persistent activation of the pathway was observed in satellite cells of the diabetic mice, which could also be reversed with a Notch inhibitor. On that basis they suggest such activation impairs satellite cell functionality in diabetic muscle. However, perhaps most significantly, most of these observations were also seen in human type 1 diabetes skeletal muscle samples, lending more support to the observations seen in mice. Commenting more widely on the study, author Thomas J. Hawke told Diabetes: "These impairments in the muscle stem cell population were profound and, more worrisome, were observed in young adulthood. Given the importance of skeletal muscle to our physical abilities and our metabolic health, deficiencies in the satellite cell population would mean a significant reduction in the ability of diabetic muscles to utilize glucose and lipids from the blood and to grow and repair following exercise. Clearly our next steps are about uncovering strategies to reverse these defects."
机译:肌肉干细胞或卫星细胞很可能在1型糖尿病中受损,因此可能导致骨骼肌萎缩,而这种萎缩通常是疾病的并发症。这是根据D'Souza等人的研究结果得出的。 (p。3053),他们研究了1型糖尿病小鼠的卫星细胞状况,以及从患有该疾病的年轻成年供体获得的人体肌肉活检样品的重要性。这组作者说,与对照组相比,运动后4周自然发展为1型糖尿病的小鼠(秋田小鼠)的耐力降低,肌肉损伤增加。对两组中的卫星细胞进行检查后发现,在患有糖尿病的小鼠中,更普遍的失败是无法产生新的肌肉细胞(肌发生),因此,卫星细胞的含量也降低了。糖尿病小鼠中肌发生的其他标志物也减少了。为了了解其中的潜在途径,作者基于Notch信号在肌发生中已确立的作用进行了研究。在糖尿病小鼠的卫星细胞中观察到该途径的持久激活,也可以用Notch抑制剂逆转。在此基础上,他们认为这种激活会损害糖尿病肌肉中的卫星细胞功能。但是,也许最重要的是,这些观察结果中的大多数也出现在人类1型糖尿病骨骼肌样本中,从而为在小鼠中观察到的观察结果提供了更多支持。作家托马斯·霍克(Thomas J. Hawke)对糖尿病研究发表了更广泛的评论:“这些肌肉干细胞群体的损害是深远的,而且在成年后的年轻人中更加令人担忧。鉴于骨骼肌对我们的身体能力和代谢的重要性健康,卫星细胞数量不足将意味着糖尿病肌肉利用血液中的葡萄糖和脂质以及运动后生长和修复的能力显着降低。显然,我们的下一步工作是寻找逆转这些缺陷的策略。”

著录项

  • 来源
    《Diabetes》 |2016年第10期|2819-2820|共2页
  • 作者

    Max Bingham;

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

  • 入库时间 2022-08-18 03:46:10

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