Apolipoprotein A-V Deficiency Results in Marked Hypertriglyceridemia Attributable to Decreased Lipolysis of Triglyceride-Rich Lipoproteins and Removal of Their Remnants

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Abstract
Objective— ApoAV, a newly discovered apoprotein, affects plasma triglyceride level. To determine how this occurs, we studied triglyceride-rich lipoprotein (TRL) metabolism in mice deficient in apoAV. Methods and Results— No significant difference in triglyceride production rate was found between apoa5 −/− mice and controls. The presence or absence of apoAV affected TRL catabolism. After the injection of 14 C-palmitate and 3 H-cholesterol labeled chylomicrons and 125 I-labeled chylomicron remnants, the disappearance of 14 C, 3 H, and 125 I was significantly slower in apoa5 −/− mice relative to controls. This was because of diminished lipolysis of TRL and the reduced rate of uptake of their remnants in apoa5 −/− mice. Observed elevated cholesterol level was caused by increased high-density lipoprotein (HDL) cholesterol in apoa5 −/− mice. VLDL from apoa5 −/− mice were poor substrate for lipoprotein lipase, and did not bind to the low-density lipoprotein (LDL) receptor as well as normal very-low-density lipoprotein (VLDL). LDL receptor levels were slightly elevated in apoa5 −/− mice consistent with lower remnant uptake rates. These alterations may be the result of the lower apoE-to-apoC ratio found in VLDL isolated from apoa5 −/− mice. Conclusions— These results support the hypothesis that the absence of apoAV slows lipolysis of TRL and the removal of their remnants by regulating their apoproteins content after secretion.

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