Caterson I D, Fuller S J, Randle P J
Biochem J. 1982 Oct 15;208(1):53-60. doi: 10.1042/bj2080053.
Intravenous administration of the fatty acid oxidation inhibitor 2-tetradecylglycidic acid had no effect on the proportion of pyruvate dehydrogenase complex in the active form in heart, diaphragm or gastrocnemius muscles or in liver, kidney or adipose tissue of fed normal rats. The compound reversed the effect of 48h starvation (which decreased the proportion of active complex) in heart muscle, partially reversed the effect of starvation in kidney, but had no effect in the other tissues listed. The compound failed to reverse the effect of alloxan-diabetes (which decreased the proportion of active complex) in any of these tissues. In perfused hearts of fed normal rats, 2-tetradecylglycidate reversed effects of palmitate (which decreased the proportion of active complex), but it had no effect in the absence of palmitate. In perfused hearts of 48h-starved rats the compound increased the proportion of active complex to that found in fed normal rats in the presence or absence of insulin. In perfused hearts of diabetic rats the compound normalized the proportion of active complex in the presence of insulin, but not in its absence. Palmitate reversed the effects of 2-tetradecylglycidate in perfused hearts of starved or diabetic rats. Evidence is given that 2-tetradecylglycidate only reverses effects of starvation and alloxan-diabetes on the proportion of active complex in heart muscle under conditions in which it inhibits fatty acid oxidation. It is concluded that effects of starvation and alloxan-diabetes on the proportion of active complex in heart muscle are dependent on fatty acid oxidation. Insulin had no effect on the proportion of active complex in hearts or diaphragms of fed or starved rats in vitro. In perfused hearts of alloxan-diabetic rats, insulin induced a modest increase in the proportion of active complex in the presence of albumin, but not in its absence.
给正常喂食的大鼠静脉注射脂肪酸氧化抑制剂2-十四烷基缩水甘油酸，对心脏、膈肌、腓肠肌、肝脏、肾脏或脂肪组织中处于活性形式的丙酮酸脱氢酶复合体比例没有影响。该化合物可逆转饥饿48小时对心肌中活性复合体比例的影响（饥饿会降低活性复合体的比例），部分逆转饥饿对肾脏的影响，但对所列的其他组织没有影响。该化合物未能逆转四氧嘧啶糖尿病对这些组织中活性复合体比例的影响（糖尿病会降低活性复合体的比例）。在正常喂食的大鼠的灌注心脏中，2-十四烷基缩水甘油酸可逆转棕榈酸的作用（棕榈酸会降低活性复合体的比例），但在没有棕榈酸的情况下则没有作用。在饥饿48小时的大鼠的灌注心脏中，无论有无胰岛素，该化合物均可使活性复合体的比例增加至正常喂食大鼠的水平。在糖尿病大鼠的灌注心脏中，该化合物在有胰岛素存在时可使活性复合体的比例恢复正常，但在没有胰岛素时则不能。棕榈酸可逆转2-十四烷基缩水甘油酸对饥饿或糖尿病大鼠灌注心脏的作用。有证据表明，2-十四烷基缩水甘油酸仅在抑制脂肪酸氧化的条件下，才能逆转饥饿和四氧嘧啶糖尿病对心肌中活性复合体比例的影响。得出的结论是，饥饿和四氧嘧啶糖尿病对心肌中活性复合体比例的影响取决于脂肪酸氧化。胰岛素对正常喂食或饥饿大鼠的心脏或膈肌中活性复合体的比例在体外没有影响。在四氧嘧啶糖尿病大鼠的灌注心脏中，胰岛素在有白蛋白存在时可使活性复合体的比例适度增加，但在没有白蛋白时则不能。
