Length of the four periods of glaciation d it could

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Unformatted text preview: ists have believed that cholesterol converted to LDL‘s. The LDL receptors thus have a dual plays a major role in heart disease because people with effect in controlling LDL levels. They are necessary to familial hypercholesterolemia, a genetic defect, have six to prevent oversynthesis of LDL‘s from VLDL remnants and eight times the normal level of cholesterol in their blood and they are necessary for the normal removal of LDL‘s from the they invariably develop heart disease. These people lack blood. With this knowledge, scientists are now well on the cell-surface receptors for low-density lipoproteins (LDL‘s), way to ward developing drugs that dramatically lower which are the fundamental carriers of blood cholesterol to cholesterol levels in people afflicted with certain forms of the body cells that use cholesterol. Without an adequate familial hypercholesterolemia. 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 slow-down 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 hyper- cholesterolemia 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 li ver in the form of a precursor, called very low-density lipoproteins (VLDL‘s), which carry triglycerides as well as relatively small amou nts 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. Nor mally, 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 114 3. In the passage, the author is primarily concerned with 5. The passage implies that if the Watan...
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This document was uploaded on 09/16/2013.

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