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SPOLIER ALERT
I have tried to include enough relevant information to come to the correct conclusion(s).
The question and answer is below (in white):
Brown and Goldstein studied people with FH. The primary defect of FH is ineffective or missing LDL receptors. How would FH affect the metabolism of cholestrol?
I. Increased intracellular cholesterol synthesis
II. Decreased activity of ACAT
III. Increased LDL cholesterol in the blood
Correct Answer: I and III Only.
Relevant information about FH and ACAT:
"[Brown and Goldstein's] work [was] on the transport of exogenous cholesterol in the bloodstream and its receptor mediated endocytosis and metabolism."
"Cholesteryl esters are synthesized from cholesterol and a fatty acid from coenzyme A through the action of acyl-CoA-cholesterol acyl transferase (ACAT). High intracellular levels of cholesterol stimulate ACAT, promoting esterification of cholesterol for storage"
My thought process: I, II, and III are all correct (I and III I correctly answered according to the answer explanation)
II. Decreased activity of ACAT
My issue with this problem is that the reason they give for option 2 being wrong isn't satisfactory:
"Statement 3 is correct...Statement 1 is correct. Also, ACAT activity increases to hydrolyze stored cholesteryl esters into free cholesterol. Statement 2 is wrong."
The only mention of ACAT is the ability to store cholesterol in the form of the cholesteryl esters. Is it okay to assume that all transferases can participate in a reverse reaction? I'm just missing where you are given the information that at low intracellular cholesterol levels ACAT has the opposite activity (breaking down, rather than storing).
If anyone has the BR bio book 2 and can elaborate that would be very helpful.
I have tried to include enough relevant information to come to the correct conclusion(s).
The question and answer is below (in white):
Brown and Goldstein studied people with FH. The primary defect of FH is ineffective or missing LDL receptors. How would FH affect the metabolism of cholestrol?
I. Increased intracellular cholesterol synthesis
II. Decreased activity of ACAT
III. Increased LDL cholesterol in the blood
Correct Answer: I and III Only.
Relevant information about FH and ACAT:
"[Brown and Goldstein's] work [was] on the transport of exogenous cholesterol in the bloodstream and its receptor mediated endocytosis and metabolism."
"Cholesteryl esters are synthesized from cholesterol and a fatty acid from coenzyme A through the action of acyl-CoA-cholesterol acyl transferase (ACAT). High intracellular levels of cholesterol stimulate ACAT, promoting esterification of cholesterol for storage"
My thought process: I, II, and III are all correct (I and III I correctly answered according to the answer explanation)
II. Decreased activity of ACAT
In the bold quote above from the passage we are told that at high intracellular levels of cholesterol stimulate ACAT which functions to store cholesterol by forming a cholesteryl ester. Because the primary source of cholesterol is intracellular production, I would assume that intracellular levels are not "high", but rather only just sufficient. For this reason I selected II as also correct.
My issue with this problem is that the reason they give for option 2 being wrong isn't satisfactory:
"Statement 3 is correct...Statement 1 is correct. Also, ACAT activity increases to hydrolyze stored cholesteryl esters into free cholesterol. Statement 2 is wrong."
The only mention of ACAT is the ability to store cholesterol in the form of the cholesteryl esters. Is it okay to assume that all transferases can participate in a reverse reaction? I'm just missing where you are given the information that at low intracellular cholesterol levels ACAT has the opposite activity (breaking down, rather than storing).
If anyone has the BR bio book 2 and can elaborate that would be very helpful.
