Gastric bypass surgery alters the mechanisms of insulin resistance in the adipose tissue of GK rats

Li,Jibin; Wang,Yong; Zhou,Yong; Liu,Jingang

doi:10.3892/mmr.2012.1053

Gastric bypass surgery alters the mechanisms of insulin resistance in the adipose tissue of GK rats

Authors:
- Jibin Li
- Yong Wang
- Yong Zhou
- Jingang Liu
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Affiliations: Department of General Surgery, Shengjing Hospital, China Medical University, Shenyang 110004, P.R. China
Published online on: August 28, 2012 https://doi.org/10.3892/mmr.2012.1053
Pages: 1111-1116

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Abstract

Roux-en-Y gastric bypass (RYGB) has become an effective treatment for type 2 diabetes mellitus (T2DM). However, the blood glucose mechanism involved remains unclear. In this study, 60 male Goto-Kakizaki (GK) rats were randomly divided into 6 groups (each with 10 rats): the GB1/2 group (treated with gastric bypass surgery), the SO1/2 group (treated with sham operation) and the CO1/2 group (with normal water consumption only). We tested expression levels of tumor necrosis factor α (TNFα) mRNA, glucose transporter 4 (GLUT4), peroxisome proliferator-activated receptor γ2 (PPARγ2) and phosphatidylinositol-3-kinase subunit p85α (PI3Kp85α) in the adipose tissues. We found that the weight, fasting blood glucose and postprandial blood glucose decreased in the GB group compared with the CO group. A total of 20 and 30 days after surgery, PPARγ2, PI3Kp85α and GLUT4 increased in the fat tissue in the GB group compared with the CO group. However, 20 days after surgery, TNFα mRNA decreased in fat tissue by 0.51 times in the GB group compared with the CO group, and serum TNFα levels showed no statistically significant difference. Fasting blood glucose and GLUT4 membrane protein were negatively correlated. In conclusion, RYGB may improve insulin resistance and treat T2DM through upregulation of the PPARγ2 protein, downregulation of TNFα mRNA transcription, through the autocrine pathway, upregulation of PI3Kp85α expression, upregulation of GLUT4 mRNA transcripts and by inducing translocation of GLUT4 in adipose tissue.

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