首页> 外文期刊>American Journal of Physiology >Fatty diabetic lung: altered alveolar structure and surfactant protein expression.
【24h】

Fatty diabetic lung: altered alveolar structure and surfactant protein expression.

机译:脂肪性糖尿病肺:肺泡结构和表面活性剂蛋白表达改变。

获取原文
获取原文并翻译 | 示例
           

摘要

Pulmonary dysfunction develops in type 2 diabetes mellitus (T2DM) in direct correlation with glycemia and is exacerbated by obesity; however, the associated structural derangement has not been quantified. We studied lungs from obese diabetic (fa/fa) male Zucker diabetic fatty (ZDF) rats at 4, 12, and 36 wk of age, before and after onset of T2DM, compared with lean nondiabetic (+/+) rats. Surfactant proteins A and C (SP-A and SP-C) immunoexpression in lung tissue was quantified at ages 14 and 18 wk, after the onset of T2DM. In fa/fa animals, lung volume was normal despite obesity. Numerous lipid droplets were visible within alveolar interstitium, lipofibroblasts, and macrophages, particularly in subpleural regions. Total triglyceride content was 136% higher. By 12 wk, septum volume was 21% higher, and alveolar duct volume was 36% lower. Capillary basement membrane was 29% thicker. Volume of lamellar bodies was 45% higher. By age 36 wk, volumes of interstitial collagen fibers, cells, and matrix were respectively 32, 25, and 80% higher, and capillary blood volume was 18% lower. ZDF rats exhibited a strain-specific increase in resistance of the air-blood diffusion barrier with age, which was exaggerated in fa/fa lungs compared with +/+ lungs. In fa/fa lungs, SP-A and SP-C expression were elevated at age 14-18 wk; the normal age-related increase in SP-A expression was accelerated, whereas SP-C expression declined with age. Thus lungs from obese T2DM animals develop many qualitatively similar changes as in type 1 diabetes mellitus but with extensive lipid deposition, altered alveolar type 2 cell ultrastructure, and surfactant protein expression patterns that suggest additive effects of hyperglycemia and lipotoxicity.
机译:肺功能不全在2型糖尿病(T2DM)中发展,与血糖直接相关,并且由于肥胖而加剧。然而,相关的结构紊乱尚未量化。与瘦型非糖尿病(+ / +)大鼠相比,我们研究了T2DM发作前后4、12和36周龄的肥胖糖尿病(fa / fa)男性祖克糖尿病脂肪(ZDF)大鼠的肺。 T2DM发作后,在14和18周龄时定量了肺组织中的表面活性蛋白A和C(SP-A和SP-C)的免疫表达。在fa / fa动物中,尽管有肥胖症,但肺活量正常。在肺泡间质,脂肪成纤维细胞和巨噬细胞内,尤其是在胸膜下区域,可见大量脂质滴。总甘油三酯含量增加了136%。到12周,隔垫体积增加21%,肺泡管体积减少36%。毛细血管基底膜厚29%。层状体的体积增加了45%。到36周龄时,间质胶原纤维,细胞和基质的体积分别增加了32%,25%和80%,毛细血管的血液体积减少了18%。 ZDF大鼠表现出随年龄增长的气血扩散屏障抵抗力的特定应变增加,与+ / +肺相比,在fa / fa肺中被夸大了。在fa / fa肺中,SP-A和SP-C的表达在14-18周龄时升高。正常的与年龄相关的SP-A表达增加加速,而SP-C的表达随年龄下降。因此,来自肥胖T2DM动物的肺部发生了许多与1型糖尿病相似的定性变化,但脂质沉积广泛,改变了2型肺泡细胞的超微结构,以及表面活性剂蛋白的表达模式提示高血糖和脂毒性的加和作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号