For some time scientists have believed that cholesterol plays a major role in heart disease because people with familial hyperch

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问题     For some time scientists have believed that cholesterol plays a major role in heart disease because people with familial hypercholesterolemia, a genetic defect, have six to eight times the normal level of cholesterol in their blood and they invariably develop heart disease. These people lack cell-surface receptors for low-density lipoproteins (LDL’s), which are the fundamental carriers of blood cholesterol to the body cells that use cholesterol. Without an adequate number of cell-surface receptors to remove LDL’s from the blood, the cholesterol-carrying LDL’s remain in the blood, increasing blood cholesterol levels. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s than normal individuals. How, scientists wondered, could a genetic mutation that causes a slowdown in the removal of LDL’s from the blood also result in an increase in the synthesis of this cholesterol-carrying protein?
    Since scientists could not experiment on human body tissue, their knowledge of familial hypercholesterolemia was severely limited. However, a breakthrough came in the laboratories of Yoshio Watanabe of Kobe University in Japan in 1980. Watanabe noticed that a male rabbit in his colony had ten times the normal concentration of cholesterol in its blood. By appropriate breeding, Watanabe obtained a strain of rabbits that had very high cholesterol levels. These rabbits spontaneously developed heart disease. To his surprise, Watanabe further found that the rabbits, like humans with familial hypercholesterolemia, lacked LDL receptors. Thus, scientists could study these Watanabe rabbits to gain a better understanding of familial hypercholesterolemia in humans.
    Prior to the breakthrough at Kobe University, it was known that LDL’s are secreted from the liver in the form of a precursor, called very low-density lipoproteins (VLDL’s) , which carry triglycerides as well as relatively small amounts of cholesterol. The triglycerides are removed from the VLDL’s by fatty and other tissues. What remains is a remnant particle that must be removed from the blood. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL remnant requires the LDL receptor. Normally, the majority of the VLDL remnants go to the liver where they bind to LDL receptors and are degraded. In the Watanabe rabbit, due to a lack of LDL receptors on liver cells, the VLDL remnants remain in the blood and are eventually converted to LDL’s. The LDL receptors thus have a dual effect in controlling LDL levels. They are necessary to prevent oversynthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood. With this knowledge, scientists are now well on the way toward developing drugs that dramatically lower cholesterol levels in people afflicted with certain forms of familial hypercholesterolemia.
According to the passage, by studying the Watanabe rabbits scientists learned that______.

选项 A、VLDL remnants are removed from the blood by LDL receptors in the liver
B、LDL’s are secreted from the liver in the form of precursors called VLDL’s
C、VLDL remnant particles contain small amounts of cholesterol
D、LDL receptors remove LDL’s from the blood

答案A

解析 事实细节题。根据题干中的by studying the Watanabe rabbits将本题出处定位于第三段第四句。本句指出,通过研究Watanabe兔子,科学家们发现,要去除超低密度脂蛋白残留物需要低密度脂蛋白受体。通过第六句可知,因为肝脏细胞缺少低密度脂蛋白受体,超低密度脂蛋白残留物就一直存在兔子的血液中,并最终转化为低密度脂蛋白。结合这两句可知,肝脏中的低密度脂蛋白受体能够去除血液中的超低密度脂蛋白残留物,故答案为[A]项。
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