Randomized clinical trial to compare the effects of preoperative oral carbohydrate versus placebo on insulin resistance after colorectal surgery

被引:136
|
作者
Wang, Z. G. [1 ]
Wang, Q. [1 ]
Wang, W. J. [1 ]
Qin, H. L. [2 ]
机构
[1] Second Mil Med Univ, Shanghai Chang Zheng Hosp, Dept Gen Surg, Shanghai, Peoples R China
[2] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 6, Shanghai 200030, Peoples R China
关键词
HOMEOSTASIS MODEL ASSESSMENT; TYPE-2; DIABETIC-PATIENTS; BETA-CELL FUNCTION; SKELETAL-MUSCLE; GLUCOSE-TRANSPORT; GLUT4; TRANSLOCATION; PHOSPHOINOSITIDE; 3-KINASE; PHOSPHATIDYLINOSITOL; 3T3-L1; ADIPOCYTES; KINASE-B;
D O I
10.1002/bjs.6963
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background: Preoperative oral carbohydrate (OCH) reduces postoperative insulin resistance (PIR). This randomized trial investigated whether this effect is related to insulin-induced activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signalling pathway. Methods: Patients with colorectal cancer scheduled for elective open resection were randomly assigned to preoperative OCH, fasting or placebo. Preoperative general well-being, insulin resistance before and immediately after surgery, and postoperative expression of PI3K, PKB, protein tyrosine kinase (PTK) and glucose transporter 4 (GLUT4) in rectus abdominis muscle were evaluated. Results: Patient and operative characteristics did not differ between groups. Subjective well-being was significantly better in OCH and placebo groups than in the fasting group, primarily because of reduced thirst (P = 0.005) and hunger (P = 0.041). PIR was significantly greater in fasting and placebo groups (P < 0.010). By the end of surgery, muscle PTK activity as well as 1:PI3K and PKB levels were significantly increased in the OCH group compared with values in fasting and placebo groups (P < 0.050), but GLUT4 expression was unaffected. Conclusion: PIR involves the PI3K/PKB signalling pathway. Preoperative OCH intake improves preoperative subjective feelings of hunger and thirst compared with fasting, while attenuating PIR by stimulation of the PI3K/PKR pathway. Registration number: NCT00755729 (http://www.clinicaltrials.gov).
引用
收藏
页码:317 / 327
页数:11
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