Population
Chylomicron-deficient mice expressing human apoB in the liver but lacking apoB synthesis in the intestine…
Comparison
Genetic modification causing chylomicron… vs Littermate controls expressing human apoB in…
Design
Preclinical
Follow-up
up to 30 days
Authors
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Animal data warrant no practice change; leaves open NEFA re-esterification as driver of human hepatic TG accumulation.
In chylomicron-deficient mice, normal plasma and hepatic triglyceride pools are maintained not by de novo lipogenesis, but by increased hepatic re-esterification of plasma non-esterified fatty acids.
Jung et al. (1999) studied this question.
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