高脂喂养大鼠分离肝细胞极低密度脂蛋白的分泌
Very-low-density-lipoprotein secretion by isolated hepatocytes of fat-fed rats.
作者信息
Kalopissis A D, Griglio S, Malewiak M I, Rozen R, Liepvre X L
出版信息
Biochem J. 1981 Aug 15;198(2):373-7. doi: 10.1042/bj1980373.
Abstract
The very-low-density-lipoprotein secretion rate of isolated hepatocytes obtained from rats fed a high-fat diet was half that of cells from control animals. In fat-fed rats, the initial cellular uptake of [l-14C]oleate in vitro was decreased by 25%, its esterification to triacylglycerols and phospholipids by 50% and its incorporation into very-low-density-lipoprotein triacylglycerols by 70%. Exogenous oleate was not the main precursor of very-low-density lipoproteins in these animals. Lipogenesis, a minor source of very-low-density lipoproteins with the control diet in our experimental conditions, was inhibited by 84% after fat-feeding. A short-term inhibition of lipogenesis in vitro did not result in a decrease in very-low-density-lipoprotein secretion rate. The results suggest that fat-feeding decreased availability of exogenous as well as endogenous fatty acids for synthesis of very-low-density lipoproteins.
摘要
从高脂饮食喂养的大鼠分离得到的肝细胞，其极低密度脂蛋白分泌率仅为对照动物细胞的一半。在高脂喂养的大鼠中，体外培养时肝细胞对[1-14C]油酸的初始摄取量降低了25%，其酯化生成三酰甘油和磷脂的量减少了50%，而其掺入极低密度脂蛋白三酰甘油中的量减少了70%。在这些动物中，外源性油酸并非极低密度脂蛋白的主要前体。在我们的实验条件下，糖脂生成是对照饮食时极低密度脂蛋白的次要来源，高脂喂养后其受到84%的抑制。体外短期抑制糖脂生成并未导致极低密度脂蛋白分泌率降低。结果表明，高脂喂养减少了外源性和内源性脂肪酸用于合成极低密度脂蛋白的可利用性。
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