Genetically modified mouse models have significantly advanced the understanding of apolipoprotein B metabolism, structure, and its role in atherogenesis and human deficiency syndromes.
Does not support clinical changes; extends preclinical apoB insights while leaving human translation open.
Over the past five years, several laboratories have used a variety of transgenic and gene-targeted mice to study apoB. These studies have helped in 1) generating new mouse models suitable for investigating the genetic and environmental factors affecting atherogenesis; 2) providing systems for investigating apoB structure/function relationships; 3) understanding the regulation of apoB gene expression in the intestine; 4) delineating a critical role for apoB expression in mouse embryonic development; 5) yielding insights into the "physiologic rationale" for the existence of the two different forms of apoB, apoB-48 and apoB-100, in mammalian metabolism; and 6) providing basic insights into mechanisms involved in the human apoB deficiency syndrome, familial hypobetalipoproteinemia.
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Kim et al. (1998) studied this question.
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