糖皮质激素对肉鸡骨骼肌糖摄取能力的影响及机制探讨

Effects of glucocorticoid on glucose intake in skeletal muscle of chicken broiers and mechanism study

利用同位素双标法,测定在NO供体硝普钠(SNP)、NO合酶(NOS)抑制剂NG-硝基、L-精氨酸甲酯(L-NAME)和糖皮质激素皮质酮(corticosterone)存在条件下,基础状态或胰岛素诱导的肉鸡离体腓骨长肌的2-脱氧葡萄糖(2-DG)转运速率。结果表明:①SNP引起肌肉基础状态和胰岛素诱导的2-DG转运速率增加,表明NO是调节骨骼肌糖代谢的一个重要细胞因子。②皮质酮引起静态肌肉2-DG转运速率增加,可能与其破坏肌纤维膜的完整性有关。③皮质酮引起肌肉胰岛素诱导的2-DG转运速率下降,加入SNP后,胰岛素机能明显改善,表明应激早期,机体NO浓度的下降,可能与糖皮质激素诱发的胰岛素抵抗有一定关系。④与体内研究不同的是,没有观察到L-NAME对离体骨骼肌2-DG转运速率的影响,表明血液动力学因素在骨骼肌糖摄取机制中同样起着非常关键的作用。

The present study was conducted to determine the effects of nitric oxide （NO） and glucocorticoid on basal and insulin-induced glucose transport rate in skeletal muscle of chicken broilers. The M. fibularis longns muscle of thirty-six broilers was incubated in vitro to measure the basal or insulin-induced 2-deoxyglucose （2-DG） transport rate combined with the NO donor sodium nitroprusside （SNP） （10mM/l）, NO syathnse （NOS） inhibitor N^G-nitro-L-arginine methyl ester （L-NAME） （2mM/l） or corticosteroue （4 mg/kg） with a double isotopes label method. The results showed that （i）SNP increased 2-DG transport in resting or insulin-stimulated muscle,which indicated that NO is a critical mediator in mechanism of glucose metabolism. （ii） It was likely that the increased 2-DG transport in resting muscle by a pharmacologically high dose of corticesterone revolved in the damaged muscle cell membrane integrity. （iii）The 2-DG transport rate stimulated by insulin was reduced when the muscle was treated with corticesterone, but the function of insulin was improved when SNP added. It indicated that acute stress in chick broilers could cause their levels of nitric oxide declined first,which correlated with their insulin resistance by glucecorticoid to a certain extent. （iv） In contrast to the effects of NOS inhibition in vivo, L-NAME failed to affect basal or insulin-stimulated 2-DG transport in isolated muscles incubatd using in vitro preparations;this suggested that hemodynamic factors were needed to fully amplify the increase in basal or insulin-stimulated glucose transport in skeletal muscle.