Scientists have created a new species of mouse suffering from atherosclerosis when fed a Western diet rich in fats. The discovery, reported in Science tomorrow * offers a model for probing the causes of a human disorder - familial combined hyperlipidemia (FCHL) - which occurs in about 2% of people in Western countries and can lead to premature coronary heart disease.
In a simple and elegant experience, Alan R. Great and his colleagues high mouse Columbia University with a human gene linked to FCHL with mice lacking receptors for several proteins that bind to low density lipoprotein ( LDL), a fat molecule to which elevated blood levels is associated with atherosclerosis. The human gene, apolipoprotein C-III is linked to high blood levels of low density lipoprotein (VLDL), also a culprit in heart disease. Thus, the offspring of mice had the worst of both worlds :. VLDL and expenses of a crippled ability to remove LDL circulating blood
Tall team fed mice a diet consisting of approximately 20% saturated fat which was also high in cholesterol. "The big surprise," said Grand, "is that both genetic defects do not simply add to each other. They were clearly synergistic." The mice four times the normal normal levels of VLDL and LDL compared to mice developed arterial clogging and earlier and more severely than did mice and genetically modified food on a regular hybrid. The finding adds weight to a theory that APOC3 and defective LDL receptors play a key role in all the high lipid levels observed in FCHL says Grand.
"There is an imaginative study," says Richard Havel, a lipid researcher at the University of California, San Francisco. But APOC3 is probably not the only villain in FCHL, which is considered from defects in several genes. yet, Havel said, the work "is a step in the right direction." the next step will be to try to breed mice with defects in several genes that mimic the human condition more closely.
* Science online subscribers can link to the full text of the report.
0 Komentar