Malewiak M I, Rozen R, Le Liepvre X, Griglio S
Laboratoire de Physiopathologie de la Nutrition, INSERM U. 177, Paris.
Diabete Metab. 1988 May-Jun;14(3):270-6.
In isolated hepatocytes of fat-fed rats, as compared to control fed animals, the cellular uptake of [1-14C] oleate and its oxidation to CO2 were similar but the incorporation of the label into water-soluble products (mainly ketone bodies) was increased by 36.6% whereas its esterification to triacylglycerols and phospholipids decreased by 36%. While endogenous ketogenesis was slightly but not significantly increased, ketone body synthesis from both 2 mM octanoate and 0.7 mM oleate was stimulated two fold. Thus, in the fatfed rats the oxidative pathway is clearly activated whereas long chain fatty acids are preferentially channelled into the oxidation pathway at the expense of esterification. Yet, hepatocyte triacylglycerol content was 3-fold higher after fat-feeding. In this regard, lysosomal triacylglycerol lipase (EC 3.1.1.3) activity, in homogenates of hepatocytes was decreased by 32% (p less than 0.01). This findings suggest a lower breakdown of endogenous triacylglycerols, which, taken together with decreased secretion of VLDL lipoprotein triacylglycerol (Kalopissis et al. Biochem. J. 198: 373, 1981) and an in vivo increased fatty acid influx to the liver may contribute to the accumulation of lipids in the livers of fat-fed rats.
与正常饮食的动物相比，在高脂喂养大鼠的分离肝细胞中，[1-¹⁴C]油酸的细胞摄取及其氧化为二氧化碳的过程相似，但标记物掺入水溶性产物（主要是酮体）的量增加了36.6%，而其酯化生成三酰甘油和磷脂的量减少了36%。虽然内源性生酮作用略有增加但不显著，但由2 mM辛酸和0.7 mM油酸生成酮体的过程被刺激了两倍。因此，在高脂喂养的大鼠中，氧化途径明显被激活，而长链脂肪酸优先被导向氧化途径，从而牺牲了酯化作用。然而，高脂喂养后肝细胞三酰甘油含量高出3倍。在这方面，肝细胞匀浆中的溶酶体三酰甘油脂肪酶（EC 3.1.1.3）活性降低了32%（p<0.01）。这一发现表明内源性三酰甘油的分解减少，这与极低密度脂蛋白三酰甘油分泌减少（卡洛皮西斯等人，《生物化学杂志》198:373，1981）以及体内脂肪酸流入肝脏增加一起，可能导致高脂喂养大鼠肝脏中脂质的积累。
