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

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• 作者：Biao He^a ; Mingyi Shi^b ; ^{shimingyi2000@yahoo.com.cn"" rel=""nofollow} ; Ling Zhang^b ; Guangzhi Li^b ; Lingxiang Zhang^b ; Hu Shao^b ; Jian Li^b ; Penghua Fang^b ; Yinping Ma^b ; Qiaojia Shi^b ; Yumei Sui^b
• 关键词：Insulin sensitivity ; Swimming ; Diabetes ; High-fat diet
• 刊名：Physiology and Behavior
• 出版年：2011
• 出版时间：1 June 2011
• 年：2011
• 卷：103
• 期：3-4
• 页码：284-289
• 全文大小：681 K

文摘

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.