Diabetes:研究发现,治疗糖尿病并发症的新方法

2018-02-27 佚名 Medicalxpress

最近的研究结果提出了一种新的方法来保护糖尿病患者免受晚期血管疾病的高风险。

最近的研究结果提出了一种新的方法来保护糖尿病患者免受晚期血管疾病的高风险。

动脉粥样硬化引起的心血管问题,动脉壁形成的斑块状病变,是2型糖尿病代谢综合征患者死亡的主要原因。

患有代谢综合症的人超过了正常范围的几个临床测量指标:血压、血糖水平、有害血脂、体重指数和腹部脂肪。

研究人员对患有代谢综合症的老鼠进行了研究。小鼠肥胖,葡萄糖耐受性受损,这是糖尿病前期的征兆。在这项研究中,一种叫做S597的胰岛素模拟合成肽可以降低血糖水平,减缓动脉粥样硬化病变的进展。

胰岛素,即使它控制糖尿病,也不能预防动脉粥样硬化。

这项研究是与诺和诺德a /S的研究合作进行的。

虽然S597是由单一的氨基酸链组成的,但看起来一点都不像胰岛素,S597仍然可以激活胰岛素受体。但是,与胰岛素不同的是,胰岛素在细胞内的转化更有选择性。

这项研究表明,当S597与胰岛素受体结合时,它优先激活一种叫做Akt的信号臂,它与降低血糖水平和其他有益效果有关。它只能被弱激活,或者甚至可能阻止另一个被称为Erk手臂的信号臂被激活,怀疑它会引起不良副作用。

动脉粥样硬化开始于血管壁出现的脂肪条纹。随着动脉粥样硬化病变的增加,由肥胖引起的炎症和免疫细胞的招募可以加速斑块的生长。

某些白血球,特别是参与炎症的单核细胞,以及被认为是血液清理组的巨噬细胞,是罪魁祸首之一。它们可以通过吞噬脂质而变得过量,并可以变成泡沫细胞。这些细胞聚集,然后死亡。病灶的核心是死细胞和其他碎片。如果它破裂,血栓就会迅速在心脏或大脑的血管中形成。

在给S597的小鼠中,病变中白细胞过多的问题似乎是在其来源:炎症单核细胞和巨噬细胞的早期产生。S597治疗的小鼠似乎不容易出现代谢综合征和肥胖引起的高白细胞计数特征。

事实上,骨髓中造血干细胞的数量降到了健康小鼠的水平。这些干细胞从胰岛素受体产生的不良信号通路中表现出较少的活性。

当完整的清除细胞数量增加时,在病变核中巨噬细胞的相对含量没有上升。S597可能使更多的巨噬细胞存活更长时间或阻碍它们的堆积。

可能是由于所有这些对白细胞的影响,病变并没有随着糖尿病和代谢综合征的快速发展而增长。

研究人员指出,S597并没有改变血浆中的胆固醇水平或全身炎症。

像他汀类药物这样降低胆固醇的药物对我们预防代谢综合征和糖尿病的心血管疾病的能力产生了巨大的影响。这项新研究的结果提供了一种概念上新颖的治疗策略,以探索作为一种额外的可能性来保护与代谢综合征和2型糖尿病相关的晚期动脉粥样硬化。

之前只有一项关于S597对生物体的影响的研究。这项新研究被认为是首次报道S597对血管系统的影响。

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    2018-03-03 丁鹏鹏
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