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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。
OBJECTIVE: To investigate the effects and mechanisms of hypoxia and epinephrine on glucose transport rate induced by insulin and contraction in skeletal muscle. METHODS: The isotope double labeling method was used to determine the 2-DG and 3-methyl glucose (3-MG) transport in isolated rat soleus muscle caused by insulin or muscle contraction in the presence of hypoxia and epinephrine s speed. RESULTS AND CONCLUSION: (1) Muscle 2-DG transport rate partially superimposed but not 3-MG under the combination of hypoxia and insulin stimulation, indicating that the increase of glucose transport rate is due to accelerated phosphorylation rather than transmembrane transport. (2) The dual hypoxia and contraction stimuli resulted in partial superposition of glucose transport rate in soleus muscle, suggesting that the mechanisms by which contraction and hypoxia regulate glucose transport may vary from muscle fiber to muscle fiber. (3) pharmacological high-dose epinephrine caused by static muscle glucose transport rate decreased, may be related to the skeletal muscle vascular wall α-adrenergic receptor and β-adrenergic receptor excited at the same time. (4) High-dose epinephrine inhibits insulin or contraction-induced 2-DG and 3-MG transport, suggesting that epinephrine may affect glucose uptake at both transmembrane and phosphorylation sites in the presence of insulin or contraction.