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Characterization of Alterations in Plasma Lipoprotein Lipid and Apoprotein Profiles Accompanying Hepatoma-induced Hyperlipidemia in Rats¹

Department of Molecular and Cell Biology, U-125, The University of Connecticut, Storrs, Connecticut 06268

Alterations in plasma lipoprotein lipid and apoprotein accompanying the hyperlipidemia of rats bearing Morris hepatoma 7288C were characterized. In tumor-bearing animals all plasma lipid classes except cholesterol ester (CE) were elevated, particularly free cholesterol (FC) and triglyceride (TG), which increased by 57 and 63%, respectively. Fasting only partially reduced the tumor-induced hyperlipidemia and had no effect on the ratios of FC/CE and TG/CE. Analysis of plasma lipoproteins revealed an elevation of VLDL, IDL, and LDL in host rats, with more than a 2-fold increase in both lipid and protein of VLDL. In contrast, the three high density fractions, HDL₂, HDL₃, and d > 1.21 g/ml, were reduced. The inverse changes in concentration of host lipoproteins of lower versus higher density indicate a defective catabolism of TG-rich lipoprotein. This possibility is supported by the analysis of apolipoprotein. The percentage of total apoprotein contributed by apo C-I and C-II was reduced in all host fractions except HDL₂, while the C-IIIs remained unchanged except for a small decrease in C-III-3 of host VLDL and a slight increase in the combined C-IIIs of HDL₂. These changes were reflected in the decreased C-I+C-II/C-III ratios of all host lipoprotein fractions. Apo E levels remained similar to control values except for a significant decrease in HDL₂. Host VLDL showed increased apo A-IV and A-I content, while A-IV was decreased in HDL₂. Changes in apo B profiles were also observed.

¹ This investigation was supported in part by research grant CA 31314 awarded by the National Cancer Institute, Department of Health and Human Services, grant 35-570 awarded by the University of Connecticut Research Foundation, and contract CB-14345-39 from the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 6/ 3/85. Revised 12/12/85. Accepted 1/ 7/86.