Basic nutritional investigationDuodenal-jejunal exclusion improves insulin resistance in type 2 diabetic rats by upregulating the hepatic insulin signaling pathway

- We performed duodenal-jejunal exclusion (DJE) on type 2 diabetic Sprague-Dawley rats with diet-induced obesity.
- This study measured hepatic IRS-2 and GLUT-2 expression in type 2 diabetic rats post-DJE.
- This study aimed to clarify the molecular mechanisms of improved glycemic control after DJE.
- DJE led to upregulate hepatic IRS-2 and GLUT-2 expression and improved insulin sensitivity in type 2 diabetic rats.

ObjectivesPrevious studies have shown duodenal-jejunal exclusion (DJE) results in the rapid resolution of type 2 diabetes; however, the underlying mechanism is unknown. This study aimed to measure the hepatic expression of insulin receptor substrate-2 (IRS-2) and glucose transporter-2 (GLUT-2) in type 2 diabetic rats post-DJE, and to investigate their roles in improved hepatic insulin resistance and glucose intolerance.MethodsType 2 diabetic Sprague-Dawley (SD) rats were randomly divided into DJE operation (DO) and control (DC) groups. Normal SD rats were also divided into DJE operation and control groups. Fasting plasma glucose and insulin concentrations were measured, and the quantitative insulin sensitivity check index (QUICKI) and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) were calculated. Eight weeks postoperation, the hepatic IRS-2 and GLUT-2 protein and mRNA levels were measured using western blotting and reverse transcription polymerase chain reaction, respectively.ResultsThe fasting blood glucose in the DO group decreased from a preoperative level of 20.21 ± 2.14 mmol/L to 8.50 ± 2.19 mmol/L (P < 0.05) 8 wk post-DJE. A change in the QUICKI revealed a dramatic increase, and HOMA-IR showed a significant decrease in the DO group (P < 0.05). Additionally, the IRS-2 and GLUT-2 protein and mRNA levels at 8 wk postoperation were significantly increased in the DO group compared with the DC group.ConclusionsDJE led to upregulated hepatic IRS-2 and GLUT-2 expression in the hepatic insulin signaling pathway and improved insulin sensitivity in type 2 diabetic rats.