Cholesterol metabolism: bile acid sequestrants: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Cholesterol metabolism: bile acid sequestrants

Sample item

A 45-year-old man with raised LDL cholesterol is started on cholestyramine. Which mechanism explains the fall in his LDL cholesterol?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Increased hepatic conversion of cholesterol to bile acids by 7-alpha-hydroxylase, with upregulation of LDL receptors

Cholestyramine binds bile acids in the gut and prevents their reabsorption, interrupting the enterohepatic circulation. The liver compensates by raising 7-alpha-hydroxylase, the rate-limiting enzyme of bile acid synthesis, which draws on hepatic cholesterol and increases LDL receptor expression. Triglycerides may rise because hepatic VLDL output increases.

Option by option

  • A. Direct inhibition of HMG-CoA reductase by the resin

    Resins are not absorbed and do not inhibit HMG-CoA reductase; that is the action of statins.

  • B. Increased faecal excretion of unabsorbed dietary triglyceride

    Resins do not cause triglyceride malabsorption in the way lipase inhibitors do.

  • C. Enhanced activity of lipoprotein lipase on VLDL

    Lipoprotein lipase activity is increased by fibrates, not resins.

  • D. Increased hepatic conversion of cholesterol to bile acids by 7-alpha-hydroxylase, with upregulation of LDL receptors (correct)

    Greater bile acid synthesis depletes hepatic cholesterol and increases LDL clearance.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is D, Increased hepatic conversion of cholesterol to bile acids by 7-alpha-hydroxylase, with upregulation of LDL receptors. Cholestyramine binds bile acids in the gut and prevents their reabsorption, interrupting the enterohepatic circulation.

Why is "Direct inhibition of HMG-CoA reductase by the resin" not the answer?

Resins are not absorbed and do not inhibit HMG-CoA reductase; that is the action of statins.

Why is "Increased faecal excretion of unabsorbed dietary triglyceride" not the answer?

Resins do not cause triglyceride malabsorption in the way lipase inhibitors do.

Why is "Enhanced activity of lipoprotein lipase on VLDL" not the answer?

Lipoprotein lipase activity is increased by fibrates, not resins.

What concept does this question test?

It tests Cholesterol metabolism: bile acid sequestrants in Biochemistry. The liver compensates by raising 7-alpha-hydroxylase, the rate-limiting enzyme of bile acid synthesis, which draws on hepatic cholesterol and increases LDL receptor expression. Triglycerides may rise because hepatic VLDL output increases.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Cholesterol metabolism: bile acid sequestrants?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.