Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 30, Issue 1, Pages 20-23Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.109.196329
Keywords
lipoprotein lipase; chylomicronemia; lipolysis; GPIHBP1
Categories
Funding
- Texas AgriLife [8738, HL090553, HL087228]
- [HL094732-01]
- [T32HL69766]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL094732, R01HL087228, P01HL090553, T32HL069766] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Objective-The risk of atherosclerosis in the setting of chylomicronemia has been a topic of debate. In this study, we examined susceptibility to atherosclerosis in Gpihbp1-deficient mice (Gpihbp1(-/-)), which manifest severe chylomicronemia as a result of defective lipolysis. Methods and Results-Gpihbp1(-/-) mice on a chow diet have plasma triglyceride and cholesterol levels of 2812 +/- 209 and 319 +/- 27 mg/dL, respectively. Even though nearly all of the lipids were contained in large lipoproteins (50 to 135 nm), the mice developed progressive aortic atherosclerosis. In other experiments, we found that both Gpihbp1-deficient apo-B48-only mice and Gpihbp1-deficient apo-B100-only mice manifest severe chylomicronemia. Thus, GPIHBP1 is required for the processing of both apo-B48-and apo-B100-containing lipoproteins. Conclusions-Chylomicronemia causes atherosclerosis in mice. Also, we found that GPIHBP1 is required for the lipolytic processing of both apo-B48- and apo-B100-containing lipoproteins. (Arterioscler Thromb Vasc Biol. 2010;30:20-23.)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available