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In Figure 13-19C, the regulation of cholesterol synthesis by LDL in normal cells is compared with that in cells from FH and JD. Why does increasing the external LDL concentration inhibit cholesterol synthesis in normal cells, but affect it only slightly in cells from FH or JD?

In Figure 13-19C, the regulation of cholesterol synthesis by LDL in normal cells is compared with that in cells from FH and JD. Why does increasing the external LDL concentration inhibit cholesterol synthesis in normal cells, but affect it only slightly in cells from FH or JD?

Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
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13-100 Cholesterol is an essential component of the plasma membrane, but people who have very high levels of cholesterol in their blood (hypercholesterolemia) tend to have heart attacks. Blood cholesterol is carried in the form of cholesterol esters in low-density lipoprotein (LDL) particles. LDL binds to a high-affinity receptor on the cell surface, enters the cell via a coated pit, and ends up in lysosomes. There its protein coat is degraded, and cholesterol esters are released and hydrolyzed to cholesterol. The released cholesterol enters the cytosol and inhibits the enzyme HMG CoA reductase, which controls the first unique step in cholesterol biosynthesis. Patients with severe hypercholesterolemia cannot remove LDL from the blood. As a result, their cells do not turn off normal cholesterol synthesis, which makes the problem worse. LDL metabolism can be conveniently divided into three stages experimentally: binding of LDL to the cell surface, internalization of LDL, and regulation of cholesterol synthesis by LDL. Skin cells from a normal person and two patients suffering from severe familial hypercholesterolemia were grown in culture and tested for LDL binding, LDL internalization, and LDL regulation of cholesterol synthesis. The results are shown in Figure 13-19. (ug/g cell protein) LDL internalized (pg/g cell protein) cholesterol synthesis (nmol/hr) 0.2 normal 0.1 0.0 tooe (A) BINDING 1.0 0.0000 0 0.2 0 50 100 (8) INTERNALIZATION normal 124 0.5 FH 50 100 0 0.0 04000 FH (C) REGULATION 0 FH normal normal 0 JD 50 100 normal JD 50 100 JD normal 50 100 0 50 100 LDL (μg/mL) LDL (g/mL) Figure 13-19 LDL metabolism in normal cells and in cells from patients with severe familial hypercholesterolemia (Problem 13-100). (A) Surface binding of LDL. Assays at 4°C allow binding but not internalization. (B) Internalization of LDL. After binding at 4°C, the cells are warmed to 37°C. Binding and uptake of LDL can be followed by labeling LDL either with ferritin particles, which can be seen by electron microscopy, or with radioactive iodine, which can be measured in a gamma counter. (C) Regulation of cholesterol synthesis by LDL B. In Figure 13-19B, internalization of LDL by normal cells increases as the external LDL concentration is increased, reaching a plateau 5-fold higher than the amount of externally bound LDL. Why does LDL enter cells from patients FH or JD at such a slow rate? C. In Figure 13-19C, the regulation of cholesterol synthesis by LDL in normal cells is compared with that in cells from FH and JD. Why does increasing the external LDL concentration inhibit cholesterol synthesis in normal cells, but affect it only slightly in cells from FH or JD? D. How would you expect the rate of cholesterol synthesis to be affected if normal cells and cells from FH or JD were incubated with cholesterol itself? (Free cholesterol crosses the plasma membrane by diffusion.
Transcribed Image Text:13-100 Cholesterol is an essential component of the plasma membrane, but people who have very high levels of cholesterol in their blood (hypercholesterolemia) tend to have heart attacks. Blood cholesterol is carried in the form of cholesterol esters in low-density lipoprotein (LDL) particles. LDL binds to a high-affinity receptor on the cell surface, enters the cell via a coated pit, and ends up in lysosomes. There its protein coat is degraded, and cholesterol esters are released and hydrolyzed to cholesterol. The released cholesterol enters the cytosol and inhibits the enzyme HMG CoA reductase, which controls the first unique step in cholesterol biosynthesis. Patients with severe hypercholesterolemia cannot remove LDL from the blood. As a result, their cells do not turn off normal cholesterol synthesis, which makes the problem worse. LDL metabolism can be conveniently divided into three stages experimentally: binding of LDL to the cell surface, internalization of LDL, and regulation of cholesterol synthesis by LDL. Skin cells from a normal person and two patients suffering from severe familial hypercholesterolemia were grown in culture and tested for LDL binding, LDL internalization, and LDL regulation of cholesterol synthesis. The results are shown in Figure 13-19. (ug/g cell protein) LDL internalized (pg/g cell protein) cholesterol synthesis (nmol/hr) 0.2 normal 0.1 0.0 tooe (A) BINDING 1.0 0.0000 0 0.2 0 50 100 (8) INTERNALIZATION normal 124 0.5 FH 50 100 0 0.0 04000 FH (C) REGULATION 0 FH normal normal 0 JD 50 100 normal JD 50 100 JD normal 50 100 0 50 100 LDL (μg/mL) LDL (g/mL) Figure 13-19 LDL metabolism in normal cells and in cells from patients with severe familial hypercholesterolemia (Problem 13-100). (A) Surface binding of LDL. Assays at 4°C allow binding but not internalization. (B) Internalization of LDL. After binding at 4°C, the cells are warmed to 37°C. Binding and uptake of LDL can be followed by labeling LDL either with ferritin particles, which can be seen by electron microscopy, or with radioactive iodine, which can be measured in a gamma counter. (C) Regulation of cholesterol synthesis by LDL B. In Figure 13-19B, internalization of LDL by normal cells increases as the external LDL concentration is increased, reaching a plateau 5-fold higher than the amount of externally bound LDL. Why does LDL enter cells from patients FH or JD at such a slow rate? C. In Figure 13-19C, the regulation of cholesterol synthesis by LDL in normal cells is compared with that in cells from FH and JD. Why does increasing the external LDL concentration inhibit cholesterol synthesis in normal cells, but affect it only slightly in cells from FH or JD? D. How would you expect the rate of cholesterol synthesis to be affected if normal cells and cells from FH or JD were incubated with cholesterol itself? (Free cholesterol crosses the plasma membrane by diffusion.
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