A Mouse Model with Features of Familial Combined Hyperlipidemia-Reference-Cited by-同舟云学术

A Mouse Model with Features of Familial Combined Hyperlipidemia

Published:1997-01-17 Issue:5298 Volume:275 Page:391-394
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Masucci-Magoulas Lori¹,Goldberg Ira J.¹,Bisgaier Charles L.²,Serajuddin Humaira¹,Francone Omar L.³,Breslow Jan L.⁴,Tall Alan R.¹

Affiliation:

1. L. Masucci-Magoulas, I. J. Goldberg, H. Serajuddin, A. R. Tall, Department of Medicine, Columbia University, 630 West 168 Street, New York, NY 10032, USA.

2. C. L. Bisgaier, Department of Vascular and Cardiac Diseases, Parke-Davis Pharmaceutical Research, 2800 Plymouth Road, Ann Arbor, MI 48105, USA.

3. O. L. Francone, Pfizer Inc., Central Research Division, Department of Metabolic Diseases, Eastern Point Road, Groton, CT 06340, USA.

4. J. L. Breslow, The Rockefeller University, Laboratory of Biochemical Genetics and Metabolism, 1230 York Avenue, New York, NY 10021, USA.

Abstract

Familial combined hyperlipidemia (FCHL) is a common inherited lipid disorder, affecting 1 to 2 percent of the population in Westernized societies. Individuals with FCHL have large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) and develop premature coronary heart disease. A mouse model displaying some of the features of FCHL was created by crossing mice carrying the human apolipoprotein C-III ( APOC3 ) transgene with mice deficient in the LDL receptor. A synergistic interaction between the apolipoprotein C-III and the LDL receptor defects produced large quantities of VLDL and LDL and enhanced the development of atherosclerosis. This mouse model may provide clues to the origin of human FCHL.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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