Whereat A F, Rabinowitz J L
Am J Cardiol. 1975 Apr;35(4):567-71. doi: 10.1016/0002-9149(75)90841-3.
The rates and products of lipid synthesis from acetate-I-14C were studied in mitochondria isolated from control and atherosclerotic rabbit aorta. More acetate was incorporated into fatty acids in the cholesterol-fed animals. The mechanism was one of chain elongation, and the resultant products were longer in chain length. The newly elongated fatty acids were esterified mostly into phospholipids, presumably those turning over most rapidly. A hypothesis is proposed for the pathogenetic sequence: Cholesterol feeding alters transport functions of the mitochondrial membranes of aortic smooth muscle cells. Respiration and redox state are altered and consequently acetate is incorporated more rapidly into fatty acids as an alternate mechanism for oxidation of the reduced form of nicotin-amide-adenine dinucleotide (NADH). Rapidly turning over phospholipids esterify these fatty acids and may transfer them ultimately to cholesterol. Esterified cholesterol is less exchangeable and commences to accumulate.
在从对照和动脉粥样硬化兔主动脉分离出的线粒体中，研究了由乙酸盐 -I-¹⁴C合成脂质的速率和产物。在喂食胆固醇的动物中，更多的乙酸盐被掺入脂肪酸中。其机制是链延长，所得产物的链长更长。新延长的脂肪酸大多被酯化为磷脂，推测是那些周转最快的磷脂。提出了一个发病机制序列的假说：喂食胆固醇会改变主动脉平滑肌细胞线粒体膜的转运功能。呼吸和氧化还原状态发生改变，因此乙酸盐作为还原型烟酰胺腺嘌呤二核苷酸（NADH）氧化的替代机制，更快地掺入脂肪酸中。快速周转的磷脂将这些脂肪酸酯化，并最终可能将它们转移到胆固醇中。酯化的胆固醇交换性较低，开始积累。
