A null mutation in the scavenger receptor gene CD36 was created in mice by targeted
homologous recombination. These mice produced no detectable CD36 protein, were viable,
and bred normally. A significant decrease in binding and uptake of oxidized low density
lipoprotein was observed in peritoneal macrophages of null mice as compared with those
from control mice. CD36 null animals had a significant increase in fasting levels of
cholesterol, nonesterified free fatty acids, and triacylglycerol. The increase in cholesterol …