Presentation by Jan L. Breslow, M.D., Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University, New York, NY., at AAAS symposium on "Gene-Diet Interactions in Coronary Heart Disease"
The mouse has become a highly useful model for the study of lipoprotein disorders and atherosclerosis. Although the mouse lipoprotein pattern is dissimilar from that of the human, through induced mutations all of the abnormal lipoprotein phenotypes in humans that are associated with atherosclerosis susceptibility have been produced in the mouse.
This has provided insights into the genes possibly responsible for these disorders in humans and has allowed more invasive studies of the pathophysiology of these disorders. The mouse as a species is highly resistant to atherosclerosis. However, several of the dislipidemias produced in the mouse have resulted in a pattern of atherosclerosis resembling what occurs in humans.
These animal models are being used to study the pathophysiology of lesion formation and the influence of candidate genes on atherosclerosis susceptibility.
Breeding the atherosclerosis prone traits onto different mouse strains has revealed large background effects, and quantitative trait locus mapping has begun to identify the differences between the strains in atherosclerosis susceptibility and resistance genes.
Finally, the mouse atherosclerosis models are being used to examine nutritional and pharmacological effects on lesion formation and progression.
Note to reporters: This is one of four fact sheets about the symposium presentation. News release also available. Contact: 214-706-1340.