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首页> 外文期刊>American Journal of Physiology >Upregulation of ACE2-ANG-(1-7)-mas axis in jejunal enterocytes of type 1 diabetic rats: Implications for glucose transport
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Upregulation of ACE2-ANG-(1-7)-mas axis in jejunal enterocytes of type 1 diabetic rats: Implications for glucose transport

机译：1型糖尿病大鼠空肠肠上皮中ACE2-ANG-（1-7）-mas轴的上调：葡萄糖转运的意义

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摘要

The inhibitory effects of the angiotensin- converting enzyme (ACE)-ANG II-angiotensin type 1 (AT 1) receptor axis on jejunal glucose uptake and the reduced expression of this system in type 1 diabetes mellitus (T1DM) have been documented previously. The ACE2-ANG-(1-7)-Mas receptor axis is thought to oppose the actions of the ACE-ANG II-AT 1 receptor axis in heart, liver, and kidney. However, the possible involvement of the ACE2- ANG-(1-7)-Mas receptor system on enhanced jejunal glucose transport in T1DM has yet to be determined. Rat everted jejunum and Caco-2 cells were used to determine the effects of ANG-(1-7) on glucose uptake and to study the ACE2-ANG-(1-7)-Mas receptor signaling pathway. Expression of target gene and protein in jejunal enterocytes and human Caco-2 cells were quantified using real-time PCR and Western blotting. T1DM increased jejunal protein and mRNA expression of ACE2 (by 59 and 173%, respectively) and Mas receptor (by 55 and 100%, respectively) in jejunum. One millimolar ANG-(1-7) reduced glucose uptake in jejunum and Caco-2 cells by 30.6 and 30.3%, respectively, effects that were abolished following addition of 1 μM A-779 (a Mas receptor blocker) or 1 μM GF- 109203X (protein kinase C inhibitor) to incubation buffer for jejunum or Caco-2 cells, respectively. Finally, intravenous treatment of animals with ANG-(1-7) significantly improved oral glucose tolerance in T1DM but not control animals. In conclusion, enhanced activity of the ACE2-ANG-(1-7)-Mas receptor axis in jejunal enterocytes is likely to moderate the T1DM-induced increase in jejunal glucose uptake resulting from downregulation of the ACE-ANG II-AT1 receptor axis. Therefore, altered activity of both ACE and ACE2 systems during diabetes will determine the overall rate of glucose transport across the jejunal epithelium.
机译：血管紧张素转换酶（ACE）-ANG II-血管紧张素1型（AT 1）受体轴对空肠葡萄糖摄取的抑制作用以及该系统在1型糖尿病（T1DM）中的表达降低已有记录。 ACE2-ANG-（1-7）-Mas受体轴被认为与ACE-ANG II-AT 1受体轴在心脏，肝脏和肾脏中的作用相反。但是，尚未确定ACE2-ANG-（1-7）-Mas受体系统可能参与T1DM中空肠葡萄糖转运的增强。使用大鼠外翻空肠和Caco-2细胞测定ANG-（1-7）对葡萄糖摄取的影响，并研究ACE2-ANG-（1-7）-Mas受体信号通路。空肠肠上皮细胞和人Caco-2细胞中靶基因和蛋白质的表达使用实时PCR和Western印迹进行定量。 T1DM使空肠中ACE2的空肠蛋白和mRNA表达（分别增加59％和173％）和Mas受体（分别增加55％和100％）。一毫摩尔ANG-（1-7）可使空肠和Caco-2细胞的葡萄糖摄取分别降低30.6％和30.3％，添加1μMA-779（一种Mas受体阻滞剂）或1μMGF- 109203X（蛋白激酶C抑制剂）分别用于空肠或Caco-2细胞的孵育缓冲液。最后，用ANG-（1-7）对动物进行静脉内治疗可显着改善T1DM的口服葡萄糖耐量，但不能改善对照动物。总之，在空肠肠上皮细胞中ACE2-ANG-（1-7）-Mas受体轴的增强活性可能会缓解由于ACE-ANG II-AT1受体轴的下调导致T1DM诱导的空肠葡萄糖摄取增加。因此，糖尿病期间ACE和ACE2系统的活性改变将决定葡萄糖在空肠上皮中的总体转运速率。

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