Augmented Carbohydrate Oxidation under Moderate Hypobaric Hypoxia Equivalent to Simulated Altitude of 2500 m
Augmented Carbohydrate Oxidation under Moderate Hypobaric Hypoxia Equivalent to Simulated Altitude of 2500 m
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DOI：
10.1620/tjem.236.163
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发表时间：
2015-07-01
影响因子：
2.2
通讯作者：
Ogita, Futoshi
中科院分区：
文献类型：
--
作者：
Goto, Kazushige;Morishima, Takuma;Ogita, Futoshi
缺氧本身刺激葡萄糖的摄取是由独立于胰岛素的机制介导的。然而，中度缺氧是否会在人类中引起类似的代谢作用尚不清楚。本研究旨在确定模拟中等海拔2500米葡萄糖负荷后的血糖调节。8名健康的年轻男性（平均±标准误差：24±1岁；171.3±1.6厘米；66.9±3.7公斤；22.8±1.0公斤/米）在低压条件（560毫米汞柱）或常压条件（745毫米汞柱）下消耗75克葡萄糖溶液。在低压舱中，氧分压随着大气压力的降低而成比例地降低，从而导致缺氧状态。葡萄糖负荷后血浆葡萄糖和血清胰岛素浓度均显著升高（P < 0.05）。然而，没有观察到显著的相互作用（条件x时间）或条件的主要效应。两种情况下血清甘油、血浆肾上腺素或血浆去甲肾上腺素浓度无显著差异。在不同条件下，(V) / dotO(2)或(V) / dotCO(2)的变化没有显著差异。然而，在低压条件下，葡萄糖负荷后90和120分钟的呼吸交换比(V / dotCO(2)/(V / dotO（2))显著升高（P < 0.05），与无压条件相比），表明中度低压缺氧增强了葡萄糖负荷后的碳水化合物氧化。总之，急性暴露于中度低压缺氧显著增强糖负荷后的碳水化合物氧化，而不影响葡萄糖或胰岛素反应。因此，短期暴露于中度低压缺氧可能对糖耐量受损的人有益。
Hypoxia itself stimulates glucose uptake mediated by a mechanism independent of insulin. However, whether moderate hypoxia causes similar metabolic effect in humans remains unclear. The present study aimed to determine glycemic regulation following glucose load at a simulated moderate altitude of 2,500 m. Eight healthy young males (mean +/- standard error: 24 +/- 1 years; 171.3 +/- 1.6 cm; 66.9 +/- 3.7 kg; 22.8 +/- 1.0 kg/m(2)) consumed 75 g of glucose solution under either hypobaric condition (560 mmHg) or normobaric condition (745 mmHg). In the hypobaric chamber, the oxygen partial pressure is proportionally reduced with a reduction of atmospheric pressure, consequently leading to the hypoxic condition. Plasma glucose and serum insulin concentrations increased significantly following glucose load in both conditions (P < 0.05). However, no significant interaction (condition x time) or main effect for condition was observed. There were no significant differences in serum glycerol, plasma epinephrine, or plasma norepinephrine concentrations between the two conditions. No significant differences between the conditions were observed in changes in (V)over dotO(2) or (V)over dotCO(2). However, the hypobaric condition showed significantly higher respiratory exchange ratio ((V)over dotCO(2)/(V)over dotO(2)) at 90 and 120 min following glucose load (P < 0.05 vs. nornnobaric condition), suggesting that carbohydrate oxidation following glucose load was enhanced in moderate hypobaric hypoxia. In conclusion, acute exposure to moderate hypobaric hypoxia significantly augmented carbohydrate oxidation following the glucose load, without affecting glucose or insulin responses. Thus, a short-time exposure to moderate hypobaric hypoxia may be beneficial for people with impaired glucose tolerance.