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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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.
Q. According to the passage, by studying the Watanabe rabbits’ scientists learned that
  • 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)
    Triglycerides are removed from VLDL's by fatty tissues
Correct answer is option 'A'. Can you explain this answer?
Verified Answer
For some time, scientists have believed that cholesterol plays a majo...
In the passage it is mentioned that "What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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.”
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Most Upvoted Answer
For some time, scientists have believed that cholesterol plays a majo...
Understanding the findings from studying Watanabe rabbits:

VLDL remnants are removed from the blood by LDL receptors in the liver:
- The passage explains that in Watanabe rabbits, the lack of LDL receptors on liver cells led to the VLDL remnants remaining in the blood.
- Normally, VLDL remnants are removed from the blood by binding to LDL receptors in the liver, where they are then degraded.
- This process is essential for maintaining normal cholesterol levels in the blood and preventing the over-synthesis of LDL's from VLDL remnants.
Therefore, based on the research conducted with Watanabe rabbits, scientists learned that the removal of VLDL remnants from the blood is facilitated by LDL receptors in the liver, highlighting the crucial role of LDL receptors in controlling cholesterol levels and preventing heart disease.
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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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer?
Question Description
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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? for UPSC 2024 is part of UPSC preparation. The Question and answers have been prepared according to the UPSC exam syllabus. Information about 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? covers all topics & solutions for UPSC 2024 Exam. Find important definitions, questions, meanings, examples, exercises and tests below for 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer?.
Solutions for 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? in English & in Hindi are available as part of our courses for UPSC. Download more important topics, notes, lectures and mock test series for UPSC Exam by signing up for free.
Here you can find the meaning of 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? defined & explained in the simplest way possible. Besides giving the explanation of 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer?, a detailed solution for 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? has been provided alongside types of 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? theory, EduRev gives you an ample number of questions to practice 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. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, 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. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) 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 over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned thata)VLDL remnants are removed from the blood by LDL receptors in the liverb)LDL's are secreted from the liver in the form of precursors called VLDL"sc)VLDL remnant particles contain small amounts of cholesterold)Triglycerides are removed from VLDL's by fatty tissuesCorrect answer is option 'A'. Can you explain this answer? tests, examples and also practice UPSC tests.
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