Bach A, Schirardin H, Weryha A, Bauer M
J Nutr. 1977 Oct;107(10):1863-70. doi: 10.1093/jn/107.10.1863.
We studied ketonemia induced in rats by a single oral load of medium-chain triglycerides (MCT) (C8:0 50.5%, C10:0 48.0%, C12:0 1.0%). Medium-chain fatty acids, rather than being incorporated into the lipids synthesized by the liver, are oxidized there, with high production of ketone bodies. Severe and long-lasting hyperketonemia developed rapidly. With increased MCT loads, ketonemia also increased, although not linearly. The level of the hyperketonemia seemed equal in the two sexes. Ingestion of MCT by fasting rats caused an additional rise in ketonemia. Long-chain triglycerides were not ketogenic, since their constituent fatty acids are incorporated into lipids and are thus less subject to oxidation. Lipids induce less severe ketonemia in genetically obese rats than in normal-weight rats.
我们研究了单次口服中链甘油三酯（MCT）（C8:0 50.5%，C10:0 48.0%，C12:0 1.0%）诱导大鼠产生酮血症的情况。中链脂肪酸并非被肝脏合成的脂质所摄取，而是在肝脏中被氧化，产生大量酮体。严重且持久的高酮血症迅速出现。随着MCT负荷增加，酮血症也会增加，尽管并非呈线性关系。高酮血症水平在两性中似乎相当。禁食大鼠摄入MCT会导致酮血症进一步升高。长链甘油三酯不产生酮，因为其组成脂肪酸被并入脂质，因此较少被氧化。与正常体重大鼠相比，脂质在遗传性肥胖大鼠中诱导的酮血症较轻。
