Chylomicronemia elicits atherosclerosis in mice--brief report

Arterioscler Thromb Vasc Biol. 2010 Jan;30(1):20-3. doi: 10.1161/ATVBAHA.109.196329. Epub 2009 Oct 8.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animal Feed
  • Animals
  • Aortic Diseases / epidemiology
  • Aortic Diseases / genetics
  • Aortic Diseases / metabolism
  • Apolipoprotein B-100 / metabolism*
  • Apolipoprotein B-48 / metabolism*
  • Atherosclerosis / epidemiology
  • Atherosclerosis / genetics
  • Atherosclerosis / metabolism*
  • Chylomicrons / metabolism*
  • Fatty Acids / metabolism
  • Female
  • Genetic Predisposition to Disease
  • Lipolysis / physiology
  • Male
  • Mice
  • Mice, Mutant Strains
  • Receptors, Lipoprotein / genetics
  • Receptors, Lipoprotein / metabolism*
  • Risk Factors
  • Triglycerides / blood

Substances

  • Apolipoprotein B-100
  • Apolipoprotein B-48
  • Chylomicrons
  • Fatty Acids
  • GPI-HBP1 protein, mouse
  • Receptors, Lipoprotein
  • Triglycerides