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甘丙肽对 2 型糖尿病大鼠肌肉胰岛素敏感性的有益作用。

Beneficial effect of galanin on insulin sensitivity in muscle of type 2 diabetic rats.

机构信息

Department of Physical Education, Anhui Defence Vacation College, Luan, Anhui Province, 237011, PR China.

出版信息

Physiol Behav. 2011 Jun 1;103(3-4):284-9. doi: 10.1016/j.physbeh.2011.02.023. Epub 2011 Feb 23.

Abstract

The aim of this study was to determine whether enhanced galanin (GAL) release induced by exercise would elevate insulin sensitivity and glucose transporter 4 (GLUT4) concentration in the plasma membranes of skeletal muscle in type 2 diabetic rats. We used M35, a GAL antagonist to antagonize the GAL function and swimming training for four weeks to increase GAL release of rats. The blood samples were analyzed for GAL and insulin concentration. The euglycemic-hyperinsulinemic clamp test was conducted for an index of glucose infusion rates. Additionally, skeletal muscle was collected and processed for GLUT4 mRNA level and GLUT4 concentration. The present findings showed that plasma GAL levels after swimming training in all three trained groups were higher compared with each sedentary control and each preswimming level. The insulin levels after swimming in both M35 treatment groups were elevated compared with each diabetic control and each pretraining level. Moreover, M35 treatment reduced glucose infusion rates compared with each diabetic control, but swimming enhanced the rates in all trained groups compared with each sedentary control. Furthermore, M35 treatment reduced GLUT4 concentration and GLUT4 mRNA levels compared with each diabetic control. The ratio of GLUT4 contents in plasma membranes to total cell membranes in both drug groups were lower compared with each diabetic control. These results suggest that endogenous GAL may enhance GLUT4 contents and promote GLUT4 transportation from intracellular membrane pools to plasma membranes. GAL is an important hormone to regulate insulin sensitivity in skeletal muscle from type 2 diabetic rats.

摘要

本研究旨在确定运动诱导的增强的甘丙肽(GAL)释放是否会提高 2 型糖尿病大鼠骨骼肌细胞膜中的胰岛素敏感性和葡萄糖转运蛋白 4(GLUT4)浓度。我们使用 M35(一种甘丙肽拮抗剂)拮抗 GAL 功能,并用游泳训练来增加大鼠的 GAL 释放。分析血液样本中的 GAL 和胰岛素浓度。进行正葡萄糖高胰岛素钳夹试验以评估葡萄糖输注率指数。此外,收集和处理骨骼肌以检测 GLUT4 mRNA 水平和 GLUT4 浓度。本研究结果表明,与所有静坐对照组和每次游泳前相比,所有三组游泳训练后的血浆 GAL 水平均升高。与每个糖尿病对照组和每次训练前相比,M35 治疗组游泳后的胰岛素水平升高。此外,M35 治疗组的葡萄糖输注率低于每个糖尿病对照组,但所有训练组的葡萄糖输注率均高于每个静坐对照组。此外,M35 治疗组降低了 GLUT4 浓度和 GLUT4 mRNA 水平,与每个糖尿病对照组相比。与每个糖尿病对照组相比,两个药物组的质膜 GLUT4 含量与总细胞膜的比值均降低。这些结果表明,内源性 GAL 可能增强 GLUT4 含量并促进 GLUT4 从细胞内膜池向质膜的转运。GAL 是调节 2 型糖尿病大鼠骨骼肌胰岛素敏感性的重要激素。

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