Wang Ya Nan , Li Zhi Gang , Zhang Chao , Li Shu De , Li Tao , Peng Jian Zhi . Homocysteine Suppress PI3K/Akt Signaling Pathway via Promoting the Expression of TRB3 in Adipose Tissue[J]. Journal of Kunming Medical University, 2017, 38(06): 15-18.
Citation: Wang Ya Nan , Li Zhi Gang , Zhang Chao , Li Shu De , Li Tao , Peng Jian Zhi . Homocysteine Suppress PI3K/Akt Signaling Pathway via Promoting the Expression of TRB3 in Adipose Tissue[J]. Journal of Kunming Medical University, 2017, 38(06): 15-18.

Homocysteine Suppress PI3K/Akt Signaling Pathway via Promoting the Expression of TRB3 in Adipose Tissue

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基金: 云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目 (2009CD213); 云南省教育厅科研基金资助项目 (2015Y398);

  • Received Date: 2017-04-19
  • Objective To build animal model of hyperhomocysteinemia (HHcy) , and to investigate the expression of TRB3 in adipose tissue and explore the effect of PI3K/Akt signaling pathway by TRB3.Me thods Twenty mice were divided into the fasting control group (n = 10) and the fasting HHcy group (n = 10) . Normal food was fed in the fasting control group. Normal food and 1.5% (mass fraction) methionine were fed in the fasting HHcy group.After the mice in every group were fed for three months.Adipose tissue in two groups was The m RNA expressions of TRB3, Akt and glucose transporter 4 (GLUT4) were detected by reverse transcription PCR.The protein expression of TRB3, Akt, p-Akt (473) and GLUT4 were measured by Western blot. Re s ults The m RNA expression of TRB3 in the fast HHcy group was increasedas compared with the control group. The m RNA expression of Akt and GLUT4 was decreased, however the result had no significant difference between two groups.Compared with the control group, the protein expression of TRB3 was increased and the protein expression of p-Akt (473) was reduced in the fast HHcy group. Whereas the protein expression of Akt and GLUT4 had no significant diffenence between two groups. Conclus ion Homocysteine may incease the uptake and utilization of glucose in adipose tissue by inhibiting PI3K/Akt signaling pathway, which may be the results of inducing the expression of TRB3 and downregulating the protein expression of p-Akt (473) and GLUT4.
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