Duodenal-Jejunal Exclusion Improves the Insulin Resistance of Type 2 Diabetic Rats by Up-Regulating the Hepatic Insulin Signaling Pathway

Ziqiang Ren, MD, Pengbo Zhang, MD, Xiaocheng Zhu, MD, Hong Zhang. Affilated Hospital of Xuzhou Medical College P.R China

Objective:Gastric bypass results in the rapid resolution of type 2 diabetes. However, the underlying mechanisms remain unclear. This study was to observe the expression of hepatic IRS-2 and GLUT-2 of type 2 diabetic rats after Duodenal-Jejunal Exclusion (DJE), and explore the possible mechanism of insulin resistance improved.

Methods:Healthy male SD rats were randomly divided into type 2 diabetes-operation group (DO group), type 2 diabetes-control group (DC group); normal-operation group (NO group) and normal-control group(NC group). Plasma glucose concentration, insulin were measured respectively at fasting condition in preoperative and postoperative 1 week, 2 weeks, 4 weeks and 8 weeks. Quantitative Insulin Sensitivity Check Index (QUICKI) was measured respectively in preoperative and postoperative 8 weeks. Protein of hepatic IRS-2 and GLUT-2 were detected by Western Blot and mRNA of hepatic IRS-2 and GLUT-2 were detected by RT-PCR in postoperative 8 weeks.

Results:The fasting blood glucose of DO group rats decreased from the preoperative (20.21±2.14) mmol/L to (8.50±2.19)mmol/L (P<0.05) at 8th week after DJE respectively. The change of QUICKI: DO group had increased dramatically, from preoperative 0.43±0.02 to 0.55±0.05 in postoperative 8 weeks (P<0.05).Compared with the DC group, in postoperative 8 weeks in the DO group, the IRS-2 protein, the GLUT-2 protein and the IRS-2 mRNA, the GLUT-2 mRNA were significantly increased respectively (Figure1,2).

Conclusion: DJE was effective in up-regulating the expression of hepatic IRS-2 and GLUT-2 in the hepatic insulin signaling pathway of type 2 diabetic rats,and meanwhile the insulin sensibility was improved.

Key words Duodenal-Jejunal Exclusion operation;Type 2 diabetes mellitus;Insulin receptor substrate-2;Glucose transporter -2;Hepatic insulin signaling

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