Aiyar A S, De A K
Strahlentherapie. 1978 Mar;154(3):208-16.
The incorporation, both in vivo and in vitro, of 14C-acetate into hepatic lipids, notably the triglyceride and free fatty acid fractions, is greatly reduced following whole-body irradiation and is indicative of significantly reduced lipogenesis. Irradiation results in a several-fold increase in fatty acid oxidation, by the liver in vitro as well as in the whole animal, during the phase of active hepatic lipid accumulation. Small increases in lipoprotein lipase activity of adipose, immediately following irradiation and up to 24 hours, and the attendant marked fall in adipose lipids are suggestive of increased mobilization of peripheral lipids during the early period. However, in view of the fact that the maximum lipid accumulation occurs very much later, inflow of extra-hepatic lipid into liver does not appear to be of major etiological significance. There is three-fold experimental evidence in support of an impairment of triglyceride transport from liver being primarily responsible for the build-up of liver lipids: (I) Triton WR-1339 induced hypertriglyceridemia is totally absent in the irradiated rat during the period when liver lipids increase significantly; (II) the rate of disappearance of radioactivity from pre-labeled hepatic lipids is considerably lower in the irradiated rats; and (III) the irradiated rats show decrease in lipoproteins of liver cell-sap and of serum, the latter being more marked and a lowered synthesis of the lipoproteins, as assessed by labeling of the protein moiety.
全身照射后，无论是在体内还是体外，14C-乙酸盐掺入肝脏脂质（尤其是甘油三酯和游离脂肪酸部分）的量都大幅减少，这表明脂肪生成显著减少。在肝脏脂质活跃积累阶段，照射会导致肝脏在体外以及整个动物体内脂肪酸氧化增加数倍。照射后立即至24小时内，脂肪组织的脂蛋白脂肪酶活性略有增加，同时脂肪组织脂质显著下降，这表明早期外周脂质动员增加。然而，鉴于最大脂质积累发生在很久之后，肝外脂质流入肝脏似乎没有主要的病因学意义。有三条实验证据支持肝脏甘油三酯转运受损是肝脏脂质积累的主要原因：（I）在肝脏脂质显著增加的时期，照射大鼠完全不存在Triton WR-1339诱导的高甘油三酯血症；（II）照射大鼠中预先标记的肝脏脂质放射性消失速率显著降低；（III）照射大鼠肝细胞液和血清中的脂蛋白减少，后者更为明显，并且通过蛋白质部分标记评估，脂蛋白合成降低。
