Author: ["Annie M. Bérard","Bernhard Föger","Alan Remaley","Robert Shamburek","Boris L. Vaisman","Glenda Talley","Beverly Paigen","Robert F. Hoyt Jr.","Santica Marcovina","H. Bryan Brewer Jr.","Silvia Santamarina-Fojo"]
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Abstract
A subset of patients with high plasma HDL concentration have enhanced rather than reduced atherosclerosis. We have developed a new transgenic mouse model overexpressing human lecithin-cholesteryl acyltransferase (LCAT) that has elevated HDL and increased diet-induced atherosclerosis. LCAT transgenic mouse HDLs are abnormal in both composition and function. Liver uptake of [3H]cholesteryl ether incorporated in transgenic mouse HDL was reduced by 41% compared with control HDL, indicating ineffective transport of HDL-cholesterol to the liver and impaired reverse cholesterol transport. Analysis of this LCAT-transgenic mouse model provides in vivo evidence for dysfunctional HDL as a potential mehanism leading to increased atherosclerosis in the presence of high plasma HDL levels.Cite this article
Bérard, A., Föger, B., Remaley, A. et al. High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithinchoesteryl acyltransferase. Nat Med 3, 744–749 (1997). https://doi.org/10.1038/nm0797-744 