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首页> 外文学位 >Chronic ethanol exposure alters expression of insulin-induced mitogen-activated protein kinases in hypertensive vascular smooth muscle cells.
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Chronic ethanol exposure alters expression of insulin-induced mitogen-activated protein kinases in hypertensive vascular smooth muscle cells.

机译：慢性乙醇暴露会改变高血压血管平滑肌细胞中胰岛素诱导的促分裂原活化蛋白激酶的表达。

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摘要

Insulin resistance is an important risk factor in development of cardiovascular diseases such as hypertension and atherosclerosis. However, the specific role of insulin resistance in the etiology of these diseases is poorly understood. On the other hand, ethanol is a potent vasoconstrictor which induces changes in mitogen activated protein kinases. We hypothesize that in hypertensive vascular smooth muscle cells (VSMCs), ethanol (ETOH) interferes with insulin action by altering mitogen activated protein kinases, the major signaling molecules implicated in the biological actions of insulin. By stimulating hypertensive (SHR) cells with 1--16 microM of insulin, ERK 1 & 2 expression increased in a time dependent manner with maximum expression occurring at 10 minutes, whereas, in normal cells (WKY), no significant increase in expression of ERK 1 & 2 was observed for at least 20 minutes. We measured expression of AKT under similar conditions. By contrast, in hypertensive cells, insulin inhibited AKT expression within the first 5 minutes. This observed insulin-induced inhibition of AKT was not observed at 10, 20, and 40 min of stimulation. On the contrary, exposing hypertensive cells chronically (24 hr) to elevated concentrations (50--800 mM) of ethanol prior to stimulating with insulin, ERK 1 & 2 expression decreased in a biphasic manner with 100 and 400 mM. Eight hundred micromoles of ethanol had maximum effect. Similarly, insulin-induced AKT decreased in hypertensive cells with maximum ETOH concentrations of 400 and 800 mM. From these data, we conclude that chronic ETOH negatively alters insulin signaling in hypertensive vascular smooth muscle cells providing an alternative molecular mechanism that may increase the risk of insulin resistance. This increased risk of insulin resistance may increase the possibility of cardiovascular diseases.
机译：胰岛素抵抗是心血管疾病如高血压和动脉粥样硬化发展的重要危险因素。但是，人们对胰岛素抵抗在这些疾病的病因中的具体作用了解甚少。另一方面，乙醇是有效的血管收缩剂，可诱导促分裂原活化的蛋白激酶发生变化。我们假设，在高血压血管平滑肌细胞（VSMC）中，乙醇（ETOH）通过改变促分裂原激活的蛋白激酶（参与胰岛素生物学作用的主要信号分子）来干扰胰岛素的作用。通过用1--16 microM的胰岛素刺激高血压（SHR）细胞，ERK 1和2的表达以时间依赖性方式增加，最大表达发生在10分钟，而在正常细胞（WKY）中，ERK 1和2的表达没有明显增加。观察到ERK 1和2至少20分钟。我们在相似条件下测量了AKT的表达。相反，在高血压细胞中，胰岛素在前5分钟内抑制AKT表达。在刺激的10、20和40分钟时未观察到这种胰岛素诱导的AKT抑制作用。相反，在用胰岛素刺激之前，将高血压细胞长期（24小时）暴露于高浓度（50--800 mM）的乙醇中，ERK 1和2的表达以双相方式分别以100和400 mM降低。八百微摩尔乙醇有最大的作用。同样，在最大ETOH浓度为400和800 mM的高血压细胞中，胰岛素诱导的AKT下降。根据这些数据，我们得出结论，慢性ETOH会对高血压血管平滑肌细胞中的胰岛素信号产生负面影响，从而提供了可能增加胰岛素抵抗风险的另一种分子机制。胰岛素抵抗风险的增加可能会增加心血管疾病的可能性。

著录项

  • 作者

    Williams, Sparkle D.;

  • 作者单位

    Tennessee State University.;

  • 授予单位 Tennessee State University.;
  • 学科 Biology Physiology.
  • 学位 M.S.
  • 年度 2010
  • 页码 57 p.
  • 总页数 57
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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