Defect in assembly process of very-low-density lipoprotein in suncus liver: an animal model of XXXX .

@entity35 @entity8151 @entity1560 @entity12218
We previously showed that @entity1560 was easily induced in suncus by starvation and that the plasma level of @entity8151 (apo B) was very low. There are three possible explanations for the low level of apo B in the animals: low synthetic rate, low secretion rate, and rapid catabolism in the circulation of apo B. We measured post-heparin lipolytic activity (lipoprotein lipase activity), which plays a key role in the catabolism of apo B-containing lipoprotein, VLDL, and found no difference between @entity35 and suncus. We also investigated the hepatic synthetic rate of apo B by liver perfusion studies. Newly synthesized apo B in the suncus liver was detected by immunoprecipitation and found to amount to 12.5% of that in @entity35 . The secretion rate of VLDL in suncus, which was estimated by intravenous injection of @entity12218 , was 13.8% of that in @entity35 . These two results suggest that there is no major defect in the secretory process. We separated Golgi apparatus from @entity35 and suncus livers, and found much fewer lipoprotein particles in suncus than in @entity35 Golgi apparatus. This evidence suggests that there is no defect in the lipolytic process or hepatic secretory process of apo B-containing lipoprotein, VLDL, but there may be a defect in the assembly process of VLDL and/or in the synthetic process of apo B in suncus. Such a defect may be one of the reasons for starvation-induced @entity1560 in suncus.
