Yeh Y Y, Zee P
J Nutr. 1976 Jan;106(1):58-67. doi: 10.1093/jn/106.1.58.
Medium-chain triglycerides (MCT) induce ketosis in several mammalian species including man. To clarify the regulation of this metabolic alteration, we fed rats either MCT or long-chain triglyceride (corn oil) and then attempted to correlate ketosis with changes in (i) concentrations of selected metabolites in plasma and (ii) the synthetic and oxidative capacities of the liver. By 1 hour after MCT feeding, plasma levels of total ketone bodies had increased 18-fold, with a maximum value reached 1 hour later. By contrast, total plasma ketones in rats fed corn oil were increased only about 2-fold at 2 hours after feeding and did not exceed this value at later intervals. Hepatic concentrations of ketone bodies also increased after MCT or corn oil feeding. Although plasma concentrations of glucose decreased and insulin increased in rats fed MCT, they were not affected by corn oil feeding. MCT-induced ketosis was depressed by glucose administration. Neither MCT nor corn oil feeding impaired utilization of glucose by the liver. Hepatic lipogenesis was suppressed 50% and 90% by MCT and corn oil feeding, respectively. A marked increase of long-chain fatty acids in plasma was observed in rats fed corn oil but not in rats fed MCT. The pronounced increase of ketones in MCT-fed rats was closely related to an elevation of octanoate. In liver slices of MCT-fed rats, ketogenesis from octanoate was 10-fold higher than from palmitate, and octanoate was oxidized 4 times more rapidly than palmitate. The ketosis of MCT-fed rats was depressed by administration of 4-pentenoic acid, a potent inhibitor of fatty acid oxidation. These results support the concept that ketosis induced by MCT stems from rapid oxidation of medium-chain fatty acids. Hyperinsulinemia, hypoglycemia and depressed lipogenesis resulting from MCT feeding appear to potentiate but not initiate ketosis.
中链甘油三酯（MCT）在包括人类在内的几种哺乳动物中会诱发酮症。为了阐明这种代谢改变的调节机制，我们给大鼠喂食MCT或长链甘油三酯（玉米油），然后试图将酮症与以下变化相关联：（i）血浆中选定代谢物的浓度；（ii）肝脏的合成和氧化能力。喂食MCT后1小时，血浆中总酮体水平增加了18倍，1小时后达到最大值。相比之下，喂食玉米油的大鼠血浆总酮体在喂食后2小时仅增加约2倍，且在随后的时间段内未超过该值。喂食MCT或玉米油后，肝脏中酮体的浓度也会增加。尽管喂食MCT的大鼠血浆葡萄糖浓度降低，胰岛素增加，但喂食玉米油对其没有影响。葡萄糖给药可抑制MCT诱导的酮症。喂食MCT和玉米油均未损害肝脏对葡萄糖的利用。喂食MCT和玉米油分别使肝脏脂肪生成抑制了50%和90%。在喂食玉米油的大鼠中观察到血浆长链脂肪酸显著增加，但喂食MCT的大鼠未出现这种情况。喂食MCT的大鼠中酮体的显著增加与辛酸的升高密切相关。在喂食MCT的大鼠肝脏切片中，辛酸生成酮体的能力比棕榈酸高10倍，辛酸的氧化速度比棕榈酸快4倍。喂食4-戊烯酸（一种有效的脂肪酸氧化抑制剂）可抑制喂食MCT的大鼠的酮症。这些结果支持了这样一种观点，即MCT诱导的酮症源于中链脂肪酸的快速氧化。喂食MCT导致的高胰岛素血症、低血糖和脂肪生成受抑制似乎会增强但不会引发酮症。
