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术前口服碳水化合物可通过激活结直肠手术后的 AMP 激活蛋白激酶来减少术后胰岛素抵抗。

Preoperative Oral Carbohydrate Reduces Postoperative Insulin Resistance by Activating AMP-Activated Protein Kinase after Colorectal Surgery.

机构信息

Department of Gastro-intestine Surgery, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.

Department of Gastro-intestine Surgery, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China,

出版信息

Dig Surg. 2020;37(5):368-375. doi: 10.1159/000505515. Epub 2020 Mar 10.

Abstract

BACKGROUND

Postoperative insulin resistance (PIR) is a common response after colorectal surgery and an independent risk factor for recovery. Preoperative oral carbohydrate (POC) has been known to reduce PIR. Herein, we investigated whether its mechanism of action involves AMP-activated protein kinase (AMPK) and mTOR/S6K1/insulin receptor substrate-1 (IRS-1) pathways.

METHODS

Patients undergoing colorectal cancer resection were randomly assigned to a POC, fasting, or placebo group. The exclusion criteria were association with diseases or intake of medication affecting insulin sensitivity. Pre- and postoperative insulin resistance, and protein phosphorylation of AMPK, mTOR, and IRS-1 in the rectus abdominis muscle were evaluated.

RESULTS

From January 2017 to December 2017, 70 patients were randomized and 63 were evaluated. No difference was found in the clinical and operative characteristics among the 3 groups. In the POC group, the levels of blood glucose, blood insulin, and homeostasis model assessment of insulin resistance were significantly lower in the POC group than the fasting and placebo groups, and the insulin sensitivity index was significantly higher. The phosphorylation of AMPK in the POC group was significantly higher than that in the other 2 groups, whereas the phosphorylation of mTOR and IRS-1 was significantly lower.

CONCLUSION

PIR involves AMPK and mTOR/S6K1/IRS-1 pathways. POC reduces PIR by the stimulation of AMPK, which suppresses the phosphorylation of mTOR/IRS-1 and attenuates PIR after colorectal resection.

摘要

背景

术后胰岛素抵抗(PIR)是结直肠手术后的常见反应,也是恢复的独立危险因素。术前口服碳水化合物(POC)已被证明可减少 PIR。在此,我们研究其作用机制是否涉及 AMP 激活的蛋白激酶(AMPK)和 mTOR/S6K1/胰岛素受体底物-1(IRS-1)途径。

方法

接受结直肠癌切除术的患者被随机分配到 POC、禁食或安慰剂组。排除标准为与影响胰岛素敏感性的疾病或药物摄入有关。评估术前和术后胰岛素抵抗以及腹直肌中 AMPK、mTOR 和 IRS-1 的蛋白磷酸化。

结果

2017 年 1 月至 2017 年 12 月,70 例患者被随机分配,63 例患者进行了评估。3 组间的临床和手术特征无差异。在 POC 组中,与禁食和安慰剂组相比,POC 组的血糖、血胰岛素和稳态模型评估的胰岛素抵抗水平显著降低,胰岛素敏感性指数显著升高。POC 组的 AMPK 磷酸化明显高于其他 2 组,而 mTOR 和 IRS-1 的磷酸化明显降低。

结论

PIR 涉及 AMPK 和 mTOR/S6K1/IRS-1 途径。POC 通过刺激 AMPK 减少 PIR,抑制 mTOR/IRS-1 的磷酸化,从而减轻结直肠切除术后的 PIR。

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