Increased sphingomyelin content of plasma lipoproteins in apolipoprotein E knockout mice reflects combined production and catabolic defects and enhances reactivity with mammalian sphingomyelinase.
Key result
Apolipoprotein E knockout mice had a significantly reduced phosphatidylcholine/sphingomyelin ratio in VLDL compared to wild-type mice (2.0 vs. 4.7), reflecting combined production and catabolic defects.
Authors
Discussion
Loading...
Member takes
Implication
Does not support clinical lipid changes; leaves open translation of VLDL defects to human atherosclerosis.
PICO
P
Population
Atherosclerosis (Apolipoprotein E knockout mouse model)
I
Intervention / Comparator
Apolipoprotein E gene knockout vs Wild-type mice
O
Primary Outcome
Phosphatidylcholine/sphingomyelin (PC/SM) ratio in VLDL, p=<0.001
Main Result
Absolute Event Rate: 2% vs 4.7%
p-value: p=<0.001
Limitations
- Animal model results may not fully translate to human pathophysiology
- Involvement of LR11 or other alternative clearance mechanisms requires further investigation
Cite This Study
Jeong et al. (1998) studied Atherosclerosis (Apolipoprotein E knockout mouse model). Apolipoprotein E gene knockout vs. Wild-type mice was evaluated on Phosphatidylcholine/sphingomyelin (PC/SM) ratio in VLDL (p=<0.001). Apolipoprotein E knockout mice had a significantly reduced phosphatidylcholine/sphingomyelin ratio in VLDL compared to wild-type mice (2.0 vs. 4.7), reflecting combined production and catabolic defects.