Lomax M A, Donaldson I A, Pogson C I
Biochem J. 1983 Aug 15;214(2):553-60. doi: 10.1042/bj2140553.
Isolated liver cells prepared from starved sheep converted palmitate into ketone bodies at twice the rate seen with cells from fed animals. Carnitine stimulated palmitate oxidation only in liver cells from fed sheep, and completely abolished the difference between fed and starved animals in palmitate oxidation. The rates of palmitate oxidation to CO2 and of octanoate oxidation to ketone bodies and CO2 were not affected by starvation or carnitine. Neither starvation nor carnitine altered the ratio of 3-hydroxybutyrate to acetoacetate or the rate of esterification of [1-14C]palmitate. Propionate, lactate, pyruvate and fructose inhibited ketogenesis from palmitate in cells from fed sheep. Starvation or the addition of carnitine decreased the antiketogenic effectiveness of gluconeogenic precursors. Propionate was the most potent inhibitor of ketogenesis, 0.8 mM producing 50% inhibition. Propionate, lactate, fructose and glycerol increased palmitate esterification under all conditions examined. Lactate, pyruvate and fructose stimulated oxidation of palmitate and octanoate to CO2. Starvation and the addition of gluconeogenic precursors stimulated apparent palmitate utilization by cells. Propionate, lactate and pyruvate decreased cellular long-chain acylcarnitine concentrations. Propionate decreased cell contents of CoA and acyl-CoA. It is suggested that propionate may control hepatic ketogenesis by acting at some point in the beta-oxidation sequence. The results are discussed in relation to the differences in the regulation of hepatic fatty acid metabolism between sheep and rats.
从饥饿绵羊制备的分离肝细胞将棕榈酸转化为酮体的速率是喂食动物细胞的两倍。肉碱仅刺激喂食绵羊肝细胞中的棕榈酸氧化，并完全消除了喂食和饥饿动物在棕榈酸氧化方面的差异。棕榈酸氧化为二氧化碳以及辛酸氧化为酮体和二氧化碳的速率不受饥饿或肉碱的影响。饥饿和肉碱均未改变3-羟基丁酸与乙酰乙酸的比例或[1-14C]棕榈酸的酯化速率。丙酸、乳酸、丙酮酸和果糖抑制喂食绵羊细胞中棕榈酸的生酮作用。饥饿或添加肉碱会降低糖异生前体的抗生酮效力。丙酸是最有效的生酮抑制剂，0.8 mM可产生50%的抑制作用。在所有检测条件下，丙酸、乳酸、果糖和甘油均增加棕榈酸酯化。乳酸、丙酮酸和果糖刺激棕榈酸和辛酸氧化为二氧化碳。饥饿和添加糖异生前体刺激细胞对棕榈酸的表观利用。丙酸、乳酸和丙酮酸降低细胞内长链酰基肉碱浓度。丙酸降低细胞内辅酶A和酰基辅酶A的含量。有人提出，丙酸可能通过在β-氧化序列的某个点起作用来控制肝脏生酮作用。结合绵羊和大鼠肝脏脂肪酸代谢调节的差异对结果进行了讨论。
