缺氧和肾上腺素对骨骼肌葡萄糖转运的影响

目的:研究缺氧和肾上腺素对胰岛素和收缩诱导的骨骼肌葡萄糖转运速率的影响和作用机理。方法:利用同位素双标法,测定缺氧和肾上腺素存在条件下,胰岛素或肌肉收缩引起大鼠离体比目鱼肌2 -脱氧葡萄糖(2 -DG)和3-甲基葡萄糖(3-MG)转运的速率。结果及结论:(1)在缺氧和胰岛素联合刺激下,肌肉2 -DG转运速率部分叠加,而3-MG则没有,表明葡萄糖转运速率增加是磷酸化加速而非跨膜转运加快所致。(2 )缺氧和收缩双重刺激导致比目鱼肌葡萄糖转运速率出现部分叠加作用,提示收缩和缺氧调节葡萄糖转运的机制可能因肌纤维不同而有所不同。(3)药理性大剂量肾上腺素引起静态肌肉葡萄糖转运速率下降,可能与骨骼肌血管壁α-肾上腺素能受体和β-肾上腺素能受体同时兴奋有关。(4)大剂量肾上腺素可抑制胰岛素或收缩诱导的2-DG和3-MG转运,表明当胰岛素或收缩存在时,肾上腺素可在跨膜和磷酸化两个位点影响葡萄糖的转运摄取。

Effects of Hypoxia and Epinephrine on Insulin- and Contraction-induced Glucose Transport in Skeletal Muscle

Objective To investigate the effects and mechanisms of hypoxia and epinephrine on insulin- and contraction-induced glucose transport rate in skeletal muscle. Methods A double isotopes label method was used to measure 2-deoxyglucose (2-DG) and 3-methylglucose (3-MG) transport rate stimulated by insulin or contraction combined with hypoxia or epinephrine in isolated rat soleus muscle in vitro. Results and Conclusions (1) Combined stimulation of hypoxia and insulin caused a partially additive effect on 2-DG but not 3-MG transport in the muscle, which indicated that it was the accelerated phosphorylation rather than the increased transport across the membrane that resulted in the higher glucose transport rate. (2) The finding that the combined stimulation of contraction and hypoxia caused a partially additive effect on glucose transport rate in soleus muscle implied that the mechanisms associated with contraction- and hypoxia-mediated glucose transport might be muscle fiber specific. (3) It was likely that the reduced glucose transport in resting muscle by a pharmacologically high dose of epinephrine revolved in the coexcitation of α- and β-adenoreceptor in muscle vessel wall. (4) Epinephrine at a large dose inhibited both 2-DG and 3-MG transport stimulated by insulin or contraction indicated that epinephrine could affect glucose transport at its two metabolic steps: the transport across the membrane and the phosphorylation, when insulin or contraction existed.