DEFECT IN ASSEMBLY PROCESS OF VERY-LOW-DENSITY LIPOPROTEIN IN SUNCUS LIVER - AN ANIMAL-MODEL OF FATTY LIVER

We previously showed that fatty liver was easily induced in suncus by starvation and that the plasma level of apolipoprotein B (ape B) was v ery low. There are three possible explanations for the low level of ap o B in the animals: low synthetic rate, low secretion rate, and rapid catabolism in the circulation of apo B. We measured post-heparin lipol ytic activity (lipoprotein lipase activity), which plays a key role in the catabolism of apo B-containing lipoprotein, VLDL, and found no di fference between rats and suncus. We also investigated the hepatic syn thetic rate of apo B by liver perfusion studies. Newly synthesized apo B in the suncus liver was detected by immunoprecipitation and found t o amount to 12.5% of that in rats. The secretion rate of VLDL in suncu s, which was estimated by intravenous injection of Triton WR1339, was 13.8% of that in rats, These two results suggest that there is no majo r defect in the secretory process. We separated Golgi apparatus from r at and suncus livers, and found much fewer lipoprotein particles in su ncus than in rat Golgi apparatus. This evidence suggests that there is no defect in the lipolytic process or hepatic secretory process of ap o B-containing lipoprotein, VLDL, but there may be a defect in the ass embly process of VLDL and/or in the synthetic process of apo B in sunc us, Such a defect may be one of the reasons for starvation-induced fat ty liver in suncus.