Abstract:
:A subset of patients with high plasma HDL concentrations 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 mechanism leading to increased atherosclerosis in the presence of high plasma HDL levels.
journal_name
Nat Medjournal_title
Nature medicineauthors
Bérard AM,Föger B,Remaley A,Shamburek R,Vaisman BL,Talley G,Paigen B,Hoyt RF Jr,Marcovina S,Brewer HB Jr,Santamarina-Fojo Sdoi
10.1038/nm0797-744subject
Has Abstractpub_date
1997-07-01 00:00:00pages
744-9issue
7eissn
1078-8956issn
1546-170Xjournal_volume
3pub_type
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