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 , 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.

　　17. In the passage, the author is primarily concerned with

　　presenting a hypothesis and describing compelling evidence in support of it

　　raising a question and describing an important discovery that led to an answer

　　showing that a certain genetically caused disease can be treated effectively with drugs

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