Yu K T, Gould M K
Diabetologia. 1981 Nov;21(5):482-8. doi: 10.1007/BF00257790.
The uptake of D-xylose by isolated rat soleus muscle (measured at 37 degrees C) was stimulated by prolonged cooling at 0 degrees C. The effect of cooling reached a maximum value after 3 h and was reversed on rewarming; reversal was temperature-dependent. Cooling stimulated xylose uptake sub-maximally compared with the effect of insulin (100 U/l). Xylose uptake in cooled muscle was further stimulated by insulin, but not by anoxia. The effect of cooling and its reversal were still demonstrable in the presence of ouabain (1 mmol/l), or when unidirectional efflux of calcium and magnesium from the muscle was induced by EDTA (5 mmol/l). The ionophore, A23187 (2.5 mg/l), depressed the effect of cooling in the presence of EDTA but not in the presence of EGTA. It is concluded that cooling disrupts and intracellular magnesium-p]ump and that muscle sugar transport is consequentially stimulated through an increase in cytoplasmic magnesium.
0℃长时间冷却可刺激离体大鼠比目鱼肌对D-木糖的摄取(在37℃下测量)。冷却效果在3小时后达到最大值,复温后逆转;逆转与温度有关。与胰岛素(100 U/l)的作用相比,冷却对木糖摄取的刺激作用未达最大值。胰岛素可进一步刺激冷却肌肉对木糖的摄取,但缺氧则无此作用。在存在哇巴因(1 mmol/l)时,或当EDTA(5 mmol/l)诱导肌肉中钙和镁的单向流出时,冷却及其逆转作用仍然明显。离子载体A23187(2.5 mg/l)在存在EDTA时可抑制冷却效果,但在存在乙二醇双四乙酸(EGTA)时则无此作用。结论是,冷却破坏了细胞内的镁泵,从而通过增加细胞质镁来刺激肌肉糖转运。