Young J C, Bryan J E, Constable S H, Tutwiler G F, Holloszy J O
Can J Physiol Pharmacol. 1984 Jul;62(7):815-8. doi: 10.1139/y84-134.
The effect of the oral hypoglycemic agent methyl palmoxirate (methyl 2-tetradecylglycidate, McN-3716), a selective inhibitor of long chain fatty acid oxidation, on the exercise capacity of normal rats was evaluated. Daily administration of 2.5 mg/kg for 7 days, or of a single dose of 10 mg/kg, of methyl palmoxirate did not affect the ability of rats to perform strenuous exercise of an intensity that caused exhaustion in less than 30 min. The ability to perform prolonged, moderately strenuous exercise of an intensity that could be maintained for more than 60 min was decreased slightly (17%) in the methyl palmoxirate treated rats. This effect appeared to be mediated by a significant reduction in initial liver glycogen content in the methyl palmoxirate treated rats. As a consequence, the methyl palmoxirate treated rats became hypoglycemic during prolonged exercise. Inhibition of fatty acid oxidation in skeletal muscle was minimal. Treatment with methyl palmoxirate protected against the development of exercise-induced ketosis. It appears that the liver is the major site of action of methyl palmoxirate when given in low dosage.
评估了口服降糖药棕榈羟肟酸甲酯（2-十四烷基缩水甘油酸甲酯，McN-3716）（一种长链脂肪酸氧化的选择性抑制剂）对正常大鼠运动能力的影响。每日给予2.5mg/kg棕榈羟肟酸甲酯，持续7天，或单次给予10mg/kg，均未影响大鼠进行强度大到可在不到30分钟内导致力竭的剧烈运动的能力。在棕榈羟肟酸甲酯处理的大鼠中，进行强度适中、可维持60分钟以上的长时间剧烈运动的能力略有下降（17%）。这种影响似乎是由棕榈羟肟酸甲酯处理的大鼠肝脏初始糖原含量显著降低介导的。因此，棕榈羟肟酸甲酯处理的大鼠在长时间运动期间出现低血糖。骨骼肌中脂肪酸氧化的抑制作用最小。棕榈羟肟酸甲酯治疗可预防运动诱导的酮症的发生。低剂量给药时，肝脏似乎是棕榈羟肟酸甲酯的主要作用部位。
