Key result
Heterozygous apolipoprotein B knockout mice had a 19% reduction in total plasma cholesterol levels compared to wild-type mice and were protected from diet-induced hypercholesterolemia, while homozygous knockout resulted in embryonic lethality.
Population
Mice (129/Sv x C57BL/6) and mouse embryos with targeted disruption of the apolipoprotein B gene
Comparison
Heterozygous and homozygous knockout of the… vs Wild-type mice
Design
Preclinical
Follow-up
up to 6 weeks (diet study)
Authors
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ApoB knockout causes murine embryonic lethality; leaves open translational relevance for human lipid disorders.
Effect estimate: 19% reduction
Absolute Event Rate: 81% vs 104%
p-value: p=<0.001
Apolipoprotein B is essential for mouse embryonic development, and its heterozygous deficiency protects against diet-induced hypercholesterolemia.
Farese et al. (1995) studied Apolipoprotein B deficiency / Hypercholesterolemia. Apolipoprotein B gene knockout vs. Wild-type mice was evaluated on Total plasma cholesterol level on a chow diet (19% reduction, p=<0.001). Heterozygous apolipoprotein B knockout mice had a 19% reduction in total plasma cholesterol levels compared to wild-type mice and were protected from diet-induced hypercholesterolemia, while homozygous knockout resulted in embryonic lethality.
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