Abstract
The role of apolipoprotein A-II (apoA-II) in atherogenesis is controversial. In vitro, apoA-II can displace apoA-I from high-density lipoprotein (HDL), activate or inhibit hepatic lipase, and inhibit the activities of the cholesterol ester transfer protein and the lecithin cholesterol acyltransferase. apoA-II has anti-atherogenic as well as proatherogenic effects. This chapter presents a study in which apoA-II–/– mice were viable and fertile. These mice had a reduction in HDL particle sizes and HDL-cholesterol levels during feeding and fasting. The reduction in HDL was due to a decreased transport rate and an increased catabolism of apoA-I and cholesterol esters. These mice displayed increased sensitivity to insulin and reduced levels of insulin, glucose, and free triglycerides. The results of this study demonstrate that apoA-II has anti-atherogenic as well as proatherogenic effects.
Published Version
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