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5 December 2013 11:26 am ,
Vol. 342 ,
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
Snake venoms are remarkably complex mixtures that can stun or kill prey within minutes. But more and more researchers...
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
Since arriving on the island of Guam in the 1940s, the brown tree snake ( Boiga irregularis ) has extirpated native...
An animal rights group known as the Nonhuman Rights Project filed lawsuits in three New York courts this week in an...
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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Mouse Model for Inherited Coronary Clogging
16 January 1997 8:00 pm
Scientists have bred a new kind of mouse that suffers from atherosclerosis when fed a high-fat Western diet. The finding, reported in tomorrow's Science,* offers a model for probing the causes of a human disorder--familial combined hyperlipidemia (FCHL)--that occurs in about 2% of individuals in Western countries and can lead to premature coronary disease.
In an elegantly simple experiment, Alan R. Tall and colleagues at Columbia University bred mice carrying a human gene linked to FCHL with mice lacking several protein receptors that bind to low-density lipoprotein (LDL), a fat molecule that at high blood levels is associated with atherosclerosis. The human gene, apolipoprotein C-III, is linked to elevated blood levels of very low density lipoprotein (VLDL), also a culprit in coronary disease. Thus the mouse offspring had the worst of both worlds: loads of circulating VLDL and a crippled ability to remove LDL from the blood.
Tall's team fed the mice a diet consisting of about 20% saturated fat that was also high in cholesterol. "The big surprise," says Tall, "was that the two genetic defects didn't just add to each other. They were markedly synergistic." The mice had a fourfold increase in VLDL and LDL levels compared to normal mice and developed arterial clogging earlier and more severely than did both normal mice and the genetically engineered hybrids on a regular diet. The finding adds weight to a theory that APOC3 and faulty LDL receptors together play a key role in the elevated lipid levels seen in FCHL, Tall says.
"It's an imaginative study," says Richard Havel, a lipid researcher at the University of California, San Francisco. But APOC3 likely isn't the only villain in FCHL, which is thought to arise from defects in several genes. Still, Havel says, 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 even more closely.