Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (2): 313-316.doi: 10.3969/j.issn.1673-8225.2011.02.030

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Expressions of phosphoinositide-3-kinase, protein kinase B and glucose transporter 4 involved in insulin signal conduction pathway in L6 rat skeletal myoblasts 

Ren Xiao-yan1, Yan Zhao-li1, Hu Kang-hong2, Su Xiu-lan3, Li Cai-ping1, Zhang Jia-ling3   

  1. 1Department of Endocrinology, 3Research Center of Clinical Medicine, Affiliated Hospital of Inner Mongolia Medical College, Hohhot  010059, Inner Mongolia Autonomous Region, China; 2Research Group of Viral RNA Structure and Function Relationships, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan  430040, Hubei Province, China
  • Received:2010-11-11 Revised:2010-12-04 Online:2011-01-08 Published:2011-01-08
  • Contact: Yan Zhao-li, Doctor, Professor, Department of Endocrinology, Affiliated Hospital of Inner Mongolia Medical College, Hohhot 010059, Inner Mongolia Autonomous Region, China aliceyzl@126.com
  • About author:Ren Xiao-yan★, Studying for master’s degree, Department of Endocrinology, Affiliated Hospital of Inner Mongolia Medical College, Hohhot 010059, Inner Mongolia Autonomous Region, China violetrenxiaoyan@ 126.com
  • Supported by:

    the Chunhui Plan, No. Z2007-1-01008; Major Issue of Affiliated Hospital of Inner Mongolia Medical College, No. NYFYZD 201005

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Abstract:

BACKGROUND: Angiotensin Ⅱ (AngⅡ) can damage the insulin signal in the downstream signaling molecules and induce insulin resistance, but the specific mechanism remain poorly understood.
OBJECTIVE: To study the effects of AngⅡ on proteins involved in insulin signal conduction pathway including phosphoinositide-3-kinase (PI3K), protein kinase B (PKB) and glucose transporter 4 (GLUT4) in L6 rat skeletal myoblasts.
METHODS: L6 rat myoblasts cultured and differentiated myotubes and were divided into 4 groups: control group, insulin group, insulin+AngⅡ group and insulin+AngⅡ+H89 group according to AngⅡ or H-89 different interventions. PI3K and PKB mRNA were detected by RT-PCR; expressions of insulin resistance substance 1 (IRS1), Ptyr-IRS1 and GLUT4 (membrane protein) were detected by immunofluorescence.
RESULTS AND CONCLUSION: The expression of PI3K mRNA were increased in the insulin, insulin+AngⅡand insulin+AngⅡ+H89 groups than that of the control group (P < 0.05). PKB total mRNA among the 4 groups was not significantly different (P > 0.05). Compared with the control group, expressions of IRS1, Ptyr-IRS1 and GLUT4 (membrane protein) were increased in the other three groups (P< 0.05). Ptyr-IRS1 and GLUT4 (membrane protein) expressions in the insulin+AngⅡ+H89 group was lower than those of the insulin group but higher than those of insulin+AngⅡ group (P < 0.05). The results demonstrated that: AngⅡ blocks insulin signaling downstream via JAK2-PKA signaling pathway, reduces GLUT4 expression and causes glucose transport hindrance, therefore, induces insulin resistance.

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