...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Differential effects of constitutively active phosphatidylinositol 3-kinase on glucose transport, glycogen synthase activity, and DNA synthesis in 3T3-L1 adipocytes.
【24h】

Differential effects of constitutively active phosphatidylinositol 3-kinase on glucose transport, glycogen synthase activity, and DNA synthesis in 3T3-L1 adipocytes.

机译：组成性活性磷脂酰肌醇3-激酶对3T3-L1脂肪细胞中葡萄糖转运，糖原合酶活性和DNA合成的差异作用。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Phosphatidylinositol 3-kinase (PI3K) activation is necessary for many insulin-induced metabolic and mitogenic responses. However, it is unclear whether PI3K activation is sufficient for any of these effects. To address this question we increased PI3K activity in differentiated 3T3-L1 adipocytes by adenovirus-mediated expression of both the inter-SH2 region of the regulatory p85 subunit of PI3K (iSH2) and the catalytic p110 alpha subunit (p110). Coexpression resulted in PI3K activity that exceeded insulin-stimulated activity by two- to fivefold in cytosol, total membranes, and the low density microsome (LDM) fraction, the site of greatest insulin stimulation. While insulin increased glucose transport 15-fold, coexpression of iSH2-p110 increased transport (5.2-) +/- 0.7-fold with a parallel increase in GLUT4 translocation to the plasma membrane. Constitutive activation of PI3K had no effect on maximally insulin-stimulated glucose transport. Neither basal nor insulin-stimulated activity of glycogen synthase or mitogen-activated protein kinase was altered by iSH2-p110 coexpression. DNA synthesis was increased twofold by insulin in control 3T3-L1 adipocytes transduced with beta-galactosidase-encoding recombinant adenovirus, while iSH2-p110 coexpression increased DNA synthesis fivefold. These data indicate that (i) increased PI3K activity is sufficient to activate some but not all metabolic responses to insulin, (ii) activation of PI3K to levels exceeding the effect of insulin in adipocyte LDM results in only a partial stimulation of glucose transport, and (iii) increased PI3K activity in the absence of growth factor or oncoprotein stimulation is a potent stimulus of DNA synthesis.
机译：磷脂酰肌醇3-激酶（PI3K）激活对于许多胰岛素诱导的代谢和有丝分裂反应都是必需的。但是，尚不清楚PI3K激活是否足以满足这些影响。为了解决这个问题，我们通过腺病毒介导的PI3K调节性p85亚基（iSH2）的SH2中间区域和催化性p110α亚基（p110）的表达，提高了分化的3T3-L1脂肪细胞中PI3K的活性。共表达导致PI3K活性在细胞溶胶，总膜和低密度微粒体（LDM）分数（最大的胰岛素刺激部位）中超过胰岛素刺激的活性两倍至五倍。尽管胰岛素使葡萄糖转运增加了15倍，但iSH2-p110的共表达增加了转运（5.2-）+/- 0.7倍，同时GLUT4向质膜的转运也平行增加。 PI3K的组成性激活对胰岛素刺激的最大葡萄糖转运没有影响。 iSH2-p110共表达不会改变糖原合酶或丝裂原激活的蛋白激酶的基础活性或胰岛素刺激的活性。在编码β-半乳糖苷酶的重组腺病毒转导的对照3T3-L1脂肪细胞中，胰岛素使DNA合成增加了两倍，而iSH2-p110共表达使DNA合成增加了五倍。这些数据表明（i）增加的PI3K活性足以激活部分而非全部的胰岛素代谢反应;（ii）将PI3K激活至超过脂肪细胞LDM中胰岛素作用的水平，只会部分刺激葡萄糖转运，并且（iii）在不存在生长因子或癌蛋白刺激的情况下增加的PI3K活性是DNA合成的有效刺激。

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